Molecular CarcinogenesisThis is an RSS file. You can use it to subscribe to this data in your favourite RSS reader, such as GoogleReader, or to display this data on your own website or blog. Subscribe to this data using MyMedWorm.Subscribe to this data using GoogleReader.Subscribe to this data using Bloglines.Subscribe to this data using MyYahoo.

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Pachymic acid inhibits cell growth and modulates arachidonic acid metabolism in nonsmall cell lung cancer A549 cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we examined the effect of PA on the proliferation of human nonsmall cell lung cancer A549 cells. Furthermore, we investigated the influences of nontoxic levels of PA on AA metabolism. Additionally, the cellular events and signal transduction pathways influenced by PA were also examined. Our results showed that PA (1) inhibited anchorage-dependent and -independent A549 growth in a concentration-dependent manner, (2) induced apoptosis and disrupted mitochondrial membrane potential in A549 cells, and at nonlethal levels, (3) decreased IL-1[beta]-induced activation of cPLA2 and COX-2, (4) suppressed IL-1[beta]-i...
Source: Molecular Carcinogenesis - November 13, 2009 Category: Molecular Biology Authors: Hui Ling, Xiaobin Jia, Yaochun Zhang, Leslie A. Gapter, Yin-shan Lim, Rajesh Agarwal, Ka-yun Ng Source Type: journals

Up regulation of GW112 Gene by NF[kappa]B promotes an antiapoptotic property in gastric cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
To clarify the regulatory mechanism of GW112 gene expression, 5[prime]-flanking region of the human GW112 gene was isolated and characterized in the present study. 5[prime]-RACE analysis showed a single transcription start site, which is located 142 nucleotides upstream of the translation initiation site. Transient transfection studies with serial deletion constructs and close examination of the sequences identified a putative NF[kappa]B binding sequence between -442 and -430, which could be responsible for efficient expression of the GW112 gene. Indeed, GW112 gene was found to be regulated by NF[kappa]B signals including ...
Source: Molecular Carcinogenesis - November 12, 2009 Category: Molecular Biology Authors: Kee K. Kim, Key S. Park, Seok B. Song, Kyoon E. Kim Source Type: journals

The tumor suppressor parafibromin is required for posttranscriptional processing of histone mRNAEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we identify a novel role of parafibromin in the regulation of replication-dependent histones. Both in vitro and in vivo analyses reveal a posttranscriptional role of parafibromin in histone mRNA processing. Downregulation of parafibromin through RNA interference or in vivo mutations lead to uncleaved histone mRNA with polyadenylated tails. These results indicate that parafibromin regulates the 3[prime] processing of histone RNA, an essential component of the cell cycle. © 2009 Wiley-Liss, Inc. (Source: Molecular Carcinogenesis)
Source: Molecular Carcinogenesis - November 11, 2009 Category: Molecular Biology Authors: Leslie J. Farber, Eric J. Kort, PengFei Wang, Jindong Chen, Bin T. Teh Source Type: journals

Silibinin inhibits human nonsmall cell lung cancer cell growth through cell-cycle arrest by modulating expression and function of key cell-cycle regulatorsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Recent studies show that silibinin possesses a strong antineoplastic potential against many cancers; however, its efficacy and underlying molecular mechanisms in nonsmall cell lung cancer (NSCLC) are not well defined. Herein, we assessed silibinin activity on prime endpoints and key molecular targets such as cell number, cell-cycle progression, and cell-cycle regulatory molecules in three cell lines representing different NSCLC subtypes, namely large cell carcinoma cells (H1299 and H460) and a bronchioalveolar carcinoma cell line (H322). Silibinin treatment (10-75 µM) inhibited cell growth and targeted cell-cycle progress...
Source: Molecular Carcinogenesis - November 11, 2009 Category: Molecular Biology Authors: Samiha Mateen, Alpna Tyagi, Chapla Agarwal, Rana P. Singh, Rajesh Agarwal Source Type: journals

Fem1b, a proapoptotic protein, mediates proteasome inhibitor-induced apoptosis of human colon cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, the proapoptotic protein Fem1b is downregulated by the proteasome in malignant colon cancer cells and mediates proteasome inhibitor-induced apoptosis of these cells. Therefore, Fem1b could represent a novel molecular target to overcome apoptosis resistance in therapy of colon cancer. © 2009 Wiley-Liss, Inc. (Source: Molecular Carcinogenesis)
Source: Molecular Carcinogenesis - November 11, 2009 Category: Molecular Biology Authors: M. Cecilia Subauste, Owen J. Sansom, Nehal Porecha, Natacha Raich, Liqin Du, Joseph F. Maher Source Type: journals

The synergistic anticancer effect of troglitazone combined with aspirin causes cell cycle arrest and apoptosis in human lung cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this report we demonstrate for the first time that, when administered in combination, TGZ and ASA can produce a strong synergistic effect in growth inhibition and G1 arrest in lung cancer CL1-0 and A549 cells. Examination by colony formation assay revealed an even more profound synergy. In Western blot, combined TGZ and ASA also could downregulate Cdk2, E2F-1, cyclin B1, cyclin D3 protein, and the ratio of phospho-Rb/Rb. Importantly, apoptosis was synergistically induced by the combination treatment, as evidenced by caspase-3 activation and PARP cleavage. The involvement of PI3K/Akt inhibition and p27 upregulation, as w...
Source: Molecular Carcinogenesis - November 11, 2009 Category: Molecular Biology Authors: Kun-Huang Yan, Chih-Jung Yao, Hwan-You Chang, Gi-Ming Lai, Ann-Lii Cheng, Shuang-En Chuang Source Type: journals

Cytochrome P450 1B1 mRNA untranslated regions interact to inhibit protein translationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study CYP1B1 mRNA and protein expression was measured in a panel of cell lines indicating that CYP1B1 regulation is altered in tumor cell lines in vitro. Interrogation of ONCOMINE revealed that CYP1B1 mRNA is not significantly overexpressed in tumors compared to normal tissues, suggesting CYP1B1 is subject to posttranscriptional control. Analysis of the CYP1B1 mRNA revealed a complex 5[prime] untranslated region (UTR) containing a small upstream open-reading frame (uORF). These features are present in mRNAs subject to translational control so the effect of the 5[prime]UTR was tested using in vitro translation in CH...
Source: Molecular Carcinogenesis - November 11, 2009 Category: Molecular Biology Authors: Andrea H. Devlin, Paul Thompson, Tracy Robson, Stephanie R. McKeown Source Type: journals

A novel strategy to inhibit FAK and IGF-1R decreases growth of pancreatic cancer xenograftsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Deregulation of insulin-like growth factor-1 receptor (IGF-1R) and focal adhesion kinase (FAK) signaling pathways plays an important role in cancer cell proliferation and metastasis. In pancreatic cancer cells, the crosstalk and compensatory mechanisms between these two pathways reduce the efficacy of the treatments that target only one of the pathways. Ablation of IGF-1R signaling by siRNA showed minimal effects on the survival and growth of pancreatic cancer cells. An increased activity of FAK pathway was seen in these cells after IGF-1R knockdown. Further inhibition of FAK pathway using Y15 significantly decreased cell ...
Source: Molecular Carcinogenesis - November 3, 2009 Category: Molecular Biology Authors: Donghang Zheng, Vita Golubovskaya, Elena Kurenova, Cheng Wood, Nicole A. Massoll, David Ostrov, William G. Cance, Steven N. Hochwald Source Type: journals

Inhibition of focal adhesion kinase and src increases detachment and apoptosis in human neuroblastoma cell linesEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Neuroblastoma is the most common extracranial solid tumor of childhood. Focal adhesion kinase (FAK) is an intracellular kinase that is overexpressed in a number of human tumors including neuroblastoma, and regulates both cellular adhesion and survival. We have studied the effects of FAK inhibition upon neuroblastoma using adenovirus-containing FAK-CD (AdFAK-CD). Utilizing an isogenic MYCN+/MYCN- neuroblastoma cell line, we found that the MYCN+ cells are more sensitive to FAK inhibition with AdFAK-CD than their MYCN negative counterparts. In addition, we have shown that phosphorylation of Src is increased in the untreated i...
Source: Molecular Carcinogenesis - November 2, 2009 Category: Molecular Biology Authors: Elizabeth A. Beierle, Xiaojie Ma, Angelica Trujillo, Elena V. Kurenova, William G. Cance, Vita M. Golubovskaya Source Type: journals

Genetic variation in MicroRNA genes and risk of oral premalignant lesionsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
MicroRNAs (miRNAs) have been reported to play a key role in oncogenesis and, recently, studies have examined the role miRNAs might play in the risk of premalignant lesions. To our knowledge, no study has investigated the association between miRNA polymorphisms and risk of oral premalignant lesions (OPLs). We genotyped 31 single nucleotide polymorphisms (SNPs) among 21 miRNA-related genes in a case-control study including 136 OPL patients and 136 matched controls. Patients with at least one variant allele of mir26a-1:rs7372209 had a significantly increased risk of OPL (OR, 2.09; 95% CI, 1.23-3.56). Likewise, patients with a...
Source: Molecular Carcinogenesis - October 22, 2009 Category: Molecular Biology Authors: Jessica Clague, Scott M. Lippman, Hushan Yang, Michelle A.T. Hildebrandt, Yuanqing Ye, J. Jack Lee, Xifeng Wu Source Type: journals

Coding microsatellite instability analysis in microsatellite unstable small intestinal adenocarcinomas identifies MARCKS as a common target of inactivationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, we herein present a cMSI profile of MSI-H small intestinal adenocarcinomas identifying MARCKS as a frequent target of mutation. Loss of MARCKS protein expression suggests a significant role of MARCKS inactivation in the pathogenesis of small intestinal adenocarcinomas. © 2009 Wiley-Liss, Inc. (Source: Molecular Carcinogenesis)
Source: Molecular Carcinogenesis - October 21, 2009 Category: Molecular Biology Authors: Sara Michel, Matthias Kloor, Sandhya Singh, Georg Gdynia, Wilfried Roth, Magnus von Knebel Doeberitz, Peter Schirmacher, Hendrik Bläker Source Type: journals

Aryl hydrocarbon nuclear translocator (hypoxia inducible factor 1[beta]) activity is required more during early than late tumor growthEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
c4 is a derivative of the mouse hepatoma cell line, Hepa-1, that harbors a mutation in the aryl hydrocarbon receptor nuclear translocator gene (Arnt, or hypoxia inducible factor 1[beta] [HIF-1[beta]]) leading to loss of activity. Clone 3 cells were generated by introducing a doxycycline-repressible Arnt expression vector into c4 cells. Clone 3 cells were injected subcutaneously into immunosuppressed mice, which were treated with doxycyline (a) throughout the growth of the subsequent tumor xenografts, or (b) from day 7 through to the end of the experiment (day 30), or not treated (c). Tumors in all groups grew exponentially...
Source: Molecular Carcinogenesis - October 12, 2009 Category: Molecular Biology Authors: S. Shi, D.Y. Yoon, K. Hodge-Bell, S. Huerta-Yepez, O. Hankinson Source Type: journals

Werner syndrome gene variants in human sarcomasEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Werner syndrome is an autosomal inherited disease that is characterized by premature aging. The gene mutated in Werner syndrome (WS), WRN, encodes both a 3[prime] [rarr] 5[prime] DNA helicase and a 3[prime] [rarr] 5[prime] DNA exonuclease. Among the WS phenotypes is an exceptionally high incidence of sarcomas. We asked whether spontaneous sarcomas, not known to be associated with WS, also harbor mutations or unreported single nucleotide polymorphisms (SNPs) in WRN. We analyzed RNA or DNA sequences within the helicase and exonuclease domains from 51 and 69 matched sarcoma and adjacent normal tissues, respectively. Among a t...
Source: Molecular Carcinogenesis - October 11, 2009 Category: Molecular Biology Authors: Jessica J. Hsu, Ashwini S. Kamath-Loeb, Eitan Glick, Brett Wallden, Karen Swisshelm, Brian P. Rubin, Lawrence A. Loeb Source Type: journals

E2F2 suppresses Myc-induced proliferation and tumorigenesisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Deregulation of E2F transcriptional activity as a result of alterations in the p16-cyclin D-Rb pathway is a hallmark of cancer. However, the roles of the different E2F family members in the process of tumorigenesis are still being elucidated. Studies in mice and humans suggest that E2F2 functions as a tumor suppressor. Here we demonstrate that E2f2 inactivation cooperates with transgenic expression of Myc to enhance tumor development in the skin and oral cavity. In fact, hemizygosity at the E2f2 locus was sufficient to increase tumor incidence in this model. Loss of E2F2 enhanced proliferation in Myc transgenic tissue but ...
Source: Molecular Carcinogenesis - October 1, 2009 Category: Molecular Biology Authors: Raju V. Pusapati, Regina L. Weaks, Robert J. Rounbehler, Mark J. McArthur, David G. Johnson Source Type: journals

Association of selected polymorphisms of CCND1, p21, and caspase8 With colorectal cancer riskEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
It has been well elucidated that the signal transduction of cell-cycle control pathway and apoptosis pathway plays an important role in the normal growth and differentiation of organisms. To test the hypothesis that mutants of key genes involved in cell-cycle regulation and apoptosis might contribute to the increased risk of colorectal cancer (CRC), a population-based case-control study was carried out in Jiashan County, Zhejiang Province. The study population was composed of 373 CRC cases and 838 controls. Five genetic variants including CCND1 G870A, p21 codon31 C/A, p21 3[prime]UTR C/T, caspase8 IVS12-19G/A, and caspase8...
Source: Molecular Carcinogenesis - September 29, 2009 Category: Molecular Biology Authors: Bing Liu, Yongjing Zhang, Mingjuan Jin, Qin Ni, Xia Liang, Xinyuan Ma, Kaiyan Yao, Qilong Li, Kun Chen Source Type: journals

Rotenone induces apoptosis in MCF-7 human breast cancer cell-mediated ROS through JNK and p38 signalingEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Rotenone is an inhibitor of the mitochondrial electron transport chain complex I, resulting in the generation of reactive oxygen species (ROS). Rotenone has been shown to display anticancer activity through the induction of apoptosis in various cancer cells. However, the underlying mechanism is still not fully understood. Here, rotenone showed a strong growth inhibitory effect against human breast cancer MCF-7 cells. DNA flow cytometric analysis, chromatin condensation, and poly (ADP-ribose) polymerase (PARP) cleavage indicated rotenone actively induced apoptosis in MCF-7 cells. The antiapoptotic protein, Bcl-2, was decrea...
Source: Molecular Carcinogenesis - September 23, 2009 Category: Molecular Biology Authors: Yea-Tzy Deng, Hsiu-Chen Huang, Jen-Kun Lin Source Type: journals

Cold-inducible RNA-binding protein contributes to human antigen R and cyclin E1 deregulation in breast cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The cell cycle regulator cyclin E1 is aberrantly expressed in a variety of human cancers. In breast cancer, elevated cyclin E1 correlates with poor outcome, as do high cytoplasmic levels of the stress-induced RNA-binding protein human antigen R (HuR). We showed previously that increased cytoplasmic HuR elevates cyclin E1 in MCF-7 breast cancer cells by stabilizing its mRNA. We show here that cold-inducible RNA-binding protein (CIRP) co-regulates cyclin E1 with HuR in breast cancer cells. CIRP had been shown to interact with HuR in Xenopus laevis oocytes and to be decreased in endometrial cancer. To investigate if human CIR...
Source: Molecular Carcinogenesis - September 22, 2009 Category: Molecular Biology Authors: Xun Guo, Yuehan Wu, Rebecca S. Hartley Source Type: journals

Aberrant DNA methylation occurs in colon neoplasms arising in the azoxymethane colon cancer modelEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Mouse models of intestinal tumors have advanced our understanding of the role of gene mutations in colorectal malignancy. However, the utility of these systems for studying the role of epigenetic alterations in intestinal neoplasms remains to be defined. Consequently, we assessed the role of aberrant DNA methylation in the azoxymethane (AOM) rodent model of colon cancer. AOM induced tumors display global DNA hypomethylation, which is similar to human colorectal cancer. We next assessed the methylation status of a panel of candidate genes previously shown to be aberrantly methylated in human cancer or in mouse models of mal...
Source: Molecular Carcinogenesis - September 22, 2009 Category: Molecular Biology Authors: Scott C. Borinstein, Melissa Conerly, Slavomir Dzieciatkowski, Swati Biswas, M. Kay Washington, Patty Trobridge, Steve Henikoff, William M. Grady Source Type: journals

Expression and function of CD9 in melanoma cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
CD9, a member of the tetraspanin family, functions as an organizer in "tetraspanin webs," through interacting with other cell adhesion molecules. It plays a role in differentiation, fertilization, and cell migration. We investigated the expression and function of CD9 in melanoma. CD9 protein expression in B16 mouse melanoma and six human melanoma cell lines was decreased compared to normal melanocytes. B16F1 clones stably overexpressing CD9 had reduced ability to form colonies in soft agar; however, paradoxically these overexpressing clones had increased ability to invade Matrigel. Similarly, transient overexpression of CD...
Source: Molecular Carcinogenesis - September 22, 2009 Category: Molecular Biology Authors: Jun Fan, Guo-Zhang Zhu, Richard M. Niles Source Type: journals

Genetic reduction of circulating insulin-like growth factor-1 inhibits azoxymethane-induced colon tumorigenesis in miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We examined markers of proliferation and apoptosis in the colons of the LID and wild-type mice to see if these were consistent with tumorigenesis. We observed a decrease in proliferation in the colons of the LID mice and an increase in apoptosis. Finally, we examined cytokine levels to determine whether IGF-1 interacts with inflammatory pathways to affect colon tumorigenesis. We observed a significant reduction in the levels of 7 out of 10 cytokines that were measured in the LID mice as compared to wild-type littermates. Results from this pilot study support the hypothesis that reductions in circulating IGF-1 levels may pr...
Source: Molecular Carcinogenesis - September 16, 2009 Category: Molecular Biology Authors: Susan E. Olivo-Marston, Stephen D. Hursting, Jackie Lavigne, Susan N. Perkins, Rami S. Maarouf, Shoshana Yakar, Curtis C. Harris Source Type: journals

N-acetyl cysteine and penicillamine induce apoptosis via the ER stress response-signaling pathwayEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study was designed to identify the genes responsible for apoptosis induction by NAC and PEN. We found that glucose-regulated protein 78 (GRP78) was upregulated in HeLa cells following treatment with NAC or PEN. GRP78 is a central regulator of endoplasmic reticulum (ER) stress and has been used as a marker of ER stress. Additionally, both the activating transcription factor 6 (ATF6) protein and X box-binding protein 1 (XBP1) mRNA were processed, which facilitates the expression of C/EBP homologous protein (CHOP), a key-signaling component of ER stress-induced apoptosis. Furthermore, the PERK-ATF4 pathway, which also in...
Source: Molecular Carcinogenesis - August 31, 2009 Category: Molecular Biology Authors: Dongyin Guan, Yingying Xu, Min Yang, Hao Wang, Xiaoming Wang, Zonghou Shen Source Type: journals

Occupational exposure to polycyclic aromatic hydrocarbons influenced neither the frequency nor the spectrum of FGFR3 mutations in bladder urothelial carcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Occupational exposure to polycyclic aromatic hydrocarbons (PAH) is associated with an increased risk of urothelial carcinoma (UC). FGFR3 is found mutated in about 70% of Ta tumors, which represent the major group at diagnosis. The influence of PAH on FGFR3 mutations and whether it is related to the emergence or shaping of these mutations is not yet known. We investigated the influence of occupational PAH on the frequency and spectrum of FGFR3 mutations. We included on 170 primary urothelial tumors from five hospitals from France. Patients (median age, 64 yr) were interviewed to gather data on occupational exposure to PAH, ...
Source: Molecular Carcinogenesis - August 30, 2009 Category: Molecular Biology Authors: Ashraf A. Bakkar, Yves Allory, Yuriko Iwatsubo, Sixtina Gil Diez de Medina, Pascale Maille, Nathalie Khreich, Audrey Riou, Karen Leroy, Dimitrios Vordos, Claude C. Abbou, Pascal Andujar, Thierry Billebaud, Soizick Chammings, Françoise Conso, Alexandre De Source Type: journals

Gastric cancer risk predisposition and prognostic significance of vascular endothelial growth factor (VEGF) gene polymorphisms - A case-control study in an Omani populationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Vascular endothelial growth factor (VEGF) plays a central role in angiogenesis, tumor growth, and metastasis. We investigated the associations between VEGF gene polymorphisms and gastric cancer (GC) risk predisposition and prognostic characteristics in an Omani population, an ethnic group which has not been studied previously. We analyzed three VEGF polymorphisms (+405 G/C, -460 T/C, and +936 C/T) by the extraction of genomic DNA from peripheral blood of 130 GC patients and 130 control subjects followed by VEGF genotyping using polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis. There we...
Source: Molecular Carcinogenesis - August 12, 2009 Category: Molecular Biology Authors: Mansour S. Al-Moundhri, Maryam Al-Nabhani, Ikram A. Burney, Abdul-Aziz Al-Farsi, Bassim Al-Bahrani Source Type: journals

Betuletol 3-methyl ether induces G2-M phase arrest and activates the sphingomyelin and MAPK pathways in human leukemia cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Betuletol 3-methyl ether (BME) is a natural phenylbenzo-[gamma]-pyrone that inhibits cell proliferation in human tumor cell lines and induces apoptotic cell death in HL-60 cells. Here we show that BME displays strong cytotoxic properties in several human leukemia cell lines (U937, K-562, THP-1, Jurkat, and Molt-3) and in cells that over-express two anti-apoptotic proteins, namely Bcl-2 and Bcl-xL. BME arrested HL-60 cells at G2-M phase of the cell cycle, which was associated with the accumulation of cyclin B1 and p21Cip1. Fluorescence microscopy experiments suggest that BME blocked the cell cycle in mitosis. The in vivo tu...
Source: Molecular Carcinogenesis - August 11, 2009 Category: Molecular Biology Authors: Sara Rubio, José Quintana, José L. Eiroa, Jorge Triana, Francisco Estévez Source Type: journals

Curcumin-induced apoptosis in ovarian carcinoma cells is p53-independent and involves p38 mitogen-activated protein kinase activation and downregulation of Bcl-2 and survivin expression and Akt signalingEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study we show that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3). In addition, p53 knockdown or p53 inhibition did not diminish curcumin killing of HEY cells, confirming p53-independent cytotoxicity. Curcumin also killed OVCA429, and SKOV3 cells grown as multicellular spheroids. Nuclear condensation and fragmentation, as well as DNA fragmentation and poly (ADP-ribose) polymerase-1 cleavage in curcumin-treated HEY cells, indicated cell death by apoptosis. Pr...
Source: Molecular Carcinogenesis - August 11, 2009 Category: Molecular Biology Authors: Jane L. Watson, Anna Greenshields, Richard Hill, Ashley Hilchie, Patrick W. Lee, Carman A. Giacomantonio, David W. Hoskin Source Type: journals

Inactivation of SNF5 cooperates with p53 loss to accelerate tumor formation in Snf5+/-;p53+/- miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Malignant rhabdoid tumors (MRTs) are poorly differentiated pediatric cancers that arise in various anatomical locations and have a very poor outcome. The large majority of these malignancies are caused by loss of function of the SNF5/INI1 component of the SWI/SNF chromatin remodeling complex. However, the mechanism of tumor development associated with SNF5 loss remains unclear. Multiple studies have demonstrated a role for SNF5 in the regulation of cyclin D1, p16INK4A, and pRbf activities suggesting it functions through the SWI/SNF complex to affect transcription of genes involved in cell cycle control. Previous studies in...
Source: Molecular Carcinogenesis - August 11, 2009 Category: Molecular Biology Authors: Jessica DelBove, Yasumichi Kuwahara, E. Lorena Mora-Blanco, Virginia Godfrey, William K. Funkhouser, Christopher D.M. Fletcher, Terry Van Dyke, Charles W.M. Roberts, Bernard E. Weissman Source Type: journals

Necdin: A multi functional protein with potential tumor suppressor role?Email this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Necdin (NDN), a member of the melanoma-associated antigen (MAGE) family of proteins was first identified in mouse stem cells of embryonal carcinoma origin induced to differentiate by treatment with retinoic acid. The human gene maps to chromosome 15q11. This imprinted region is implicated in the pathogenesis of Prader-Willi syndrome (PWS), a neurodevelopmental disorder, where NDN is one of multiple genes silenced by deletion, maternal uniparental disomy or translocation. Due to this association, much interest has focused on the role of NDN in neuronal development and differentiation. However, a considerable number of studi...
Source: Molecular Carcinogenesis - July 22, 2009 Category: Molecular Biology Authors: Emma J. Chapman, Margaret A. Knowles Source Type: journals

Involvement of p53 in oroxylin A-induced apoptosis in cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we investigate whether p53 is involved in oroxylin A-triggered viability inhibition and apoptosis induction in cancer cells. In a panel of different cancer cell lines, more potent inhibitory effects of oroxylin A were observed in wtp53 cells than those in mtp53 or p53-null cells. Moreover, p53-siRNA-transfected HepG2 cells showed lower levels of apoptosis induced by oroxylin A than control-siRNA-transfected cells. Likewise, after oroxylin A treatment, p53-null K-562 cells displayed promoted apoptosis rate when transfected with wtp53 plasmid. Western blot and real-time RT-PCR assay revealed that oroxylin A ma...
Source: Molecular Carcinogenesis - July 21, 2009 Category: Molecular Biology Authors: Rong Mu, Qi Qi, Hongyan Gu, Jia Wang, Yong Yang, Jingjing Rong, Wei Liu, Na Lu, Qidong You, Qinglong Guo Source Type: journals

Colocalization of MnSOD expression in response to oxidative stressEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we investigated the expression and localization of MnSOD in response to the exposure to bile salts in an esophageal epithelial cell line. Het-1A cells were seeded at 5 × 105 and 107 and incubated with taurocholate, cholate, glycochlate, deoxycholate, and the mixture of these bile salts. Mitochondria and cytoplasma were separated, and the expression and localization of MnSOD was determined by Western blot and immunocytochemical assay. Proliferation rates were strongly inhibited in the groups with taurocholate and bile salts mixture at 4 h, with 0.367 ± 0.042 and 0.396 ± 0.046, respectively, compared to 0.6...
Source: Molecular Carcinogenesis - July 21, 2009 Category: Molecular Biology Authors: Yan Li, Nathaniel P. Reuter, Xuanshe Li, Qiaohong Liu, Jingwen Zhang, Robert C.G. Martin Source Type: journals

Adenylosuccinate synthetase 1 gene is a novel target of deletion in lung adenocarcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Tobacco smoke consists of numerous carcinogens whose effect on lung tumor development includes the induction of mutations in key genes as well as the induction of chromosome instability (CIN). Consequently, carcinogen-induced mouse lung adenocarcinomas (LAC) display many more recurrent site- and chromosome-specific changes in DNA copy number compared with noninduced LAC. Here we identified the Adenylosuccinate synthetase 1 (Adss1) gene located on distal chromosome 12q as a focus of bi-allelic or homozygous deletion (HD) in LAC. HDs of Adss1 were detected in 10 out of 84 carcinogen-induced mouse primary LAC and mouse LAC ce...
Source: Molecular Carcinogenesis - July 14, 2009 Category: Molecular Biology Authors: Joshua C. Miller, Daniel C. Blake Jr, Christopher R. Herzog Source Type: journals

PI3K signaling maintains c-myc expression to regulate transcription of E2F1 in pancreatic cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study we demonstrate that PI3K signaling controls transcription of the E2F1 gene and show that E2F1 is essential for S-phase progression of PDAC cells. On the molecular level, PI3K signaling controls c-myc protein abundance in a glycogen synthase kinase-3 (GSK3)-dependent fashion. c-myc binds to the E-box of the E2F1 gene in PDAC cells and this binding is under control of the PI3K-signaling pathway. Together, we demonstrate that PI3K-GSK3-dependent control of c-myc protein expression is connected to the transcription of the E2F1 gene in PDAC cells, leading to S-phase progression of the cell cycle. © 2009 Wiley-Lis...
Source: Molecular Carcinogenesis - July 13, 2009 Category: Molecular Biology Authors: Carolin Schild, Matthias Wirth, Maximilian Reichert, Roland M. Schmid, Dieter Saur, Günter Schneider Source Type: journals

MSH6 G39E polymorphism and CpG island methylator phenotype in colon cancerEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The objective of our investigation was to evaluate associations between the MSH6 G39E (116G>A) polymorphism and CpG island methylator phenotype (CIMP) and BRAF V600E mutations in tumors from a sample of 1048 individuals with colon cancer and 1964 controls from Utah, Northern California, and Minnesota. The G39E polymorphism (rs1042821) was determined by the five prime nuclease assay. CIMP was determined by methylation-specific polymerase chain reaction (PCR) of CpG islands in MLH1, methylated in tumors (MINT)1, MINT2, MINT31, and CDKN2A. The BRAF V600E mutation was determined by sequencing exon 15. In microsatellite stable ...
Source: Molecular Carcinogenesis - July 6, 2009 Category: Molecular Biology Authors: Karen Curtin, Wade S. Samowitz, Roger K. Wolff, Bette J. Caan, Cornelia M. Ulrich, John D. Potter, Martha L. Slattery Source Type: journals

Insulin-like growth factor type I receptor gene expression and obesity in esophageal adenocarcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The objective of this exploratory study was to evaluate the role of the insulin-like growth factor I receptor (IGF-IR) in esophageal adenocarcinoma (EADC). Using quantitative PCR, we studied IGF-IR mRNA expression in 52 well-characterized surgically resected EADC and matched histologically normal esophageal tissues, and examined IGF-IR expression levels in relation to clinicopathologic characteristics, body mass index (BMI), and the common IGF-IR polymorphism (G1013A), recently proposed to modify risk of obesity for EADC. Expression levels of IGF-IR mRNA were not significantly different between EADC and matched histologica...
Source: Molecular Carcinogenesis - July 5, 2009 Category: Molecular Biology Authors: Ronghua Zhao, Kimberley Macdonald, Alan G. Casson Source Type: journals

Desipramine inhibits the growth of a mouse skin squamous cell carcinoma cell line and affects glucocorticoid receptor-mediated transcriptionEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The purpose of this study was to examine the effect of tricyclic antidepressant desipramine (DMI) on the growth inhibition and translocation of the glucocorticoid receptor (GR) from the cytoplasm to the nucleus in cancerous and noncancerous cell lines and the effect of DMI on GR-mediated transcription. Nontumorigenic, immortalized keratinocytes cell line (3PC), papilloma (MT1/2), and squamous cell carcinoma (Ca3/7) cell lines were initially used to study the cell growth inhibition by DMI. Although, the growth of all three cell lines was suppressed by DMI, it was more effective in Ca3/7 cells. Therefore, we next examined th...
Source: Molecular Carcinogenesis - July 4, 2009 Category: Molecular Biology Authors: Tatsuya Kinjo, Piotr Kowalczyk, Magdalena Kowalczyk, Zbigniew Walaszek, Tadashi Nishimaki, Thomas J. Slaga, Margaret Hanausek Source Type: journals

Epigenetic inactivation of Homeobox A5 gene in nonsmall cell lung cancer and its relationship with clinicopathological featuresEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this study, we have investigated the methylation status of the promoter region of the HOXA5 gene in nonsmall cell lung cancers (NSCLCs) using nested and standard methylation-specific PCR (MSP) and correlated the methylation status with clinicopathological features. With standard MSP analysis, HOXA5 methylation were found in 113 (81.3%) of 139 NSCLCs and 72 (51.8%) in their corresponding nonmalignant lung tissues. RT-PCR and immunohistochemical analysis showed that HOXA5 methylation correlates with gene expression. Moreover, in the patients with stage I disease, HOXA5 methylation was more frequent in smokers than in neve...
Source: Molecular Carcinogenesis - June 24, 2009 Category: Molecular Biology Authors: Dong-Sun Kim, Min-Jin Kim, Ji-Yun Lee, Su-Man Lee, Jun-Young Choi, Ghil-Suk Yoon, Yeon-Kyung Na, Hae-Sook Hong, Sang-Geol Kim, Jin-Eun Choi, Shin-Yeop Lee, Jae-Yong Park Source Type: journals

Two genetic variants in prostate stem cell antigen and gastric cancer susceptibility in a chinese populationEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We examined genotypes and haplotypes of PSCA, rs2294008C/T and rs2976392G/A in 716 patients with cardia gastric carcinoma (CGC), 1020 patients with noncardia gastric carcinoma (NCGC), and 1020 controls. We found that individuals with at least one copy of the rs2294008T allele (CT or TT genotype) had an elevated risk for developing NCGC compared with those without this allele (OR = 1.35, 95% CI = 1.13-1.61). Individuals with at least one copy of the rs2976392A allele (GA or AA genotype) had nonsignificantly increased risk for NCGC compared with those without this allele (OR = 1.20, 95% CI = 1.01-1.43). Stratification analys...
Source: Molecular Carcinogenesis - June 23, 2009 Category: Molecular Biology Authors: Chen Wu, Guanghai Wang, Ming Yang, Liming Huang, Dianke Yu, Wen Tan, Dongxin Lin Source Type: journals

Inositol hexaphosphate downregulates both constitutive and ligand-induced mitogenic and cell survival signaling, and causes caspase-mediated apoptotic death of human prostate carcinoma PC-3 cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Constitutively active mitogenic and prosurvival signaling cascades due to aberrant expression and interaction of growth factors and their receptors are well documented in human prostate cancer (PCa). Epidermal growth factor (EGF) and insulin-like growth factor-1 (IGF-1) are potent mitogens that regulate proliferation and survival of PCa cells via autocrine and paracrine loops involving both mitogen-activated protein kinase (MAPK)- and Akt-mediated signaling. Accordingly, here we assessed the effect of inositol hexaphosphate (IP6) on constitutive and ligand (EGF and IGF-1)-induced biological responses and associated signali...
Source: Molecular Carcinogenesis - June 17, 2009 Category: Molecular Biology Authors: Mallikarjuna Gu, Komal Raina, Chapla Agarwal, Rajesh Agarwal Source Type: journals

Activation of p53/p21/PUMA alliance and disruption of PI-3/Akt in multimodal targeting of apoptotic signaling cascades in cervical cancer cells by a pentacyclic triterpenediol from Boswellia serrataEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
This study reports the apoptotic cell death in human cervical cancer HeLa and SiHa cells by a pentacyclic triterpenediol (TPD) from Boswellia serrata by a mechanism different from reported in HL-60 cells. It caused oxidative stress by early generation of nitric oxide and reactive oxygen species that robustly up regulated time-dependent expression of p53/p21/PUMA while conversely abrogating phosphatidylinositol-3-kinase (PI3K)/Akt pathways in parallel. TPD also decreased the expression of PI3K/pAkt, ERK1/2, NF-[kappa]B/Akt signaling cascades which coordinately contribute to cancer cell survival through these distinct pathwa...
Source: Molecular Carcinogenesis - June 17, 2009 Category: Molecular Biology Authors: Shashi Bhushan, Fayaz Malik, Ajay Kumar, Harpreet Kaur Isher, Indu Pal Kaur, Subhash Chandra Taneja, Jaswant Singh Source Type: journals

Using cells devoid of RAS proteins as tools for drug discoveryEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Mutational activation of RAS proteins occurs in nearly 30% of all human tumors. To date direct pharmacological inhibition of RAS oncoproteins has not been possible. As a consequence, current strategies are focusing on the development of inhibitors that target those kinases acting downstream of RAS proteins, including those of the RAF/MEK/ERK and PI3K/AKT pathways. Most of these inhibitors have undesired off-target effects that mask the potential therapeutic effect of blocking their targeted kinases. To facilitate the screening of selective inhibitors, we have generated lines of mouse embryonic fibroblasts that lack endogen...
Source: Molecular Carcinogenesis - June 11, 2009 Category: Molecular Biology Authors: Jelena Urosevic, Eleanor Y.M. Sum, Victoria Moneo, Matthias Drosten, Alma Dhawahir, Mercedes Becerra, Amancio Carnero, Mariano Barbacid Source Type: journals

The suppression of MAD1 by AKT-mediated phosphorylation activates MAD1 target genes transcriptionEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
MAX dimerization protein 1 (MAD1) is a transcription suppressor that antagonizes MYC-mediated transcription activation, and the inhibition mechanism occurs mainly through the competition of target genes' promoter MYC binding sites by MAD1. The promoter binding proteins switch between MYC and MAD1 affects cell proliferation and differentiation. However, little is known about MAD1's regulation process in cancer cells. Here, we present evidence that AKT inhibits MAD1-mediated transcription repression by physical interaction with and phosphorylation of MAD1. Phosphorylation reduces the binding affinity between MAD1 and its tar...
Source: Molecular Carcinogenesis - June 11, 2009 Category: Molecular Biology Authors: Chao-Kai Chou, Dung-Fang Lee, Hui-Lung Sun, Long-Yuan Li, Chun-Yi Lin, Wei-Chien Huang, Jung-Mao Hsu, Hsu-Ping Kuo, Hirohito Yamaguchi, Ying-Nai Wang, Mo Liu, Hsin-Yi Wu, Pao-Chi Liao, Chia-Jui Yen, Mien-Chie Hung Source Type: journals

Cellular dichotomy between anchorage-independent growth responses to bFGF and TPA reflects molecular switch in commitment to carcinogenesisEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
We have investigated gene expression patterns underlying reversible and irreversible anchorage-independent growth (AIG) phenotypes to identify more sensitive markers of cell transformation for studies directed at interrogating carcinogenesis responses. In JB6 mouse epidermal cells, basic fibroblast growth factor (bFGF) induces an unusually efficient and reversible AIG response, relative to 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced AIG which is irreversible. The reversible and irreversible AIG phenotypes are characterized by largely nonoverlapping global gene expression profiles. However, a subset of differentiall...
Source: Molecular Carcinogenesis - June 11, 2009 Category: Molecular Biology Authors: Katrina M. Waters, Ruimin Tan, Lee K. Opresko, Ryan D. Quesenberry, Somnath Bandyopadhyay, William B. Chrisler, Thomas J. Weber Source Type: journals

Differential alterations in metabolic pattern of the spliceosomal uridylic acid-rich small nuclear RNAs (UsnRNAs) during malignant transformation of 20-methylcholanthrene-induced mouse CNCI-PM-20 embryonic fibroblastsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Differential alterations of the spliceosomal Uridylic acid rich small nuclear RNAs (UsnRNAs) (U1, U2, U4, U5, and U6) are reported to be associated with cellular proliferation and development, but definitive information is scarce and also elusive. An attempt is made in this study to analyze the metabolic patterns of major spliceosomal UsnRNAs, during tumor development, in an in vitro carcinogenesis model of 20-methylcholanthrene (MCA)-transformed Swiss Mouse Embryonic Fibroblast (MEF), designated as CNCI-PM-20. MEF cells, after treatment with 20-MCA, progressed through a sequence of passages with distinct and heritable cha...
Source: Molecular Carcinogenesis - June 5, 2009 Category: Molecular Biology Authors: Sudeshna Mukherjee, Sugata Manna, Pratima Mukherjee, Chinmay K. Panda Source Type: journals

Effect of polymorphisms in the 3[prime] untranslated region (3[prime]-UTR) of vascular endothelial growth factor gene on gastric cancer and peptic ulcer diseases in JapanEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
A complex interaction of host genetic and environmental factors may be relevant in the development of Helicocobacter pylori-related gastric carcinogenesis. We investigated the effect of vascular endothelial growth factor (VEGF) gene polymorphisms on the risk of gastric cancer (GC) and peptic ulcer diseases in a Japanese population. The G1612A(rs10434) and C936T(rs3025039) polymorphisms in the 3[prime] untranslated region (3[prime]-UTR) of VEGF gene were genotyped in a total of 844 subjects including 385 GC, 143 ulcer including 98 gastric ulcer (GU), 45 duodenal ulcer (DU), and 316 nonulcer subjects. The 1612A carrier held ...
Source: Molecular Carcinogenesis - June 3, 2009 Category: Molecular Biology Authors: Tomomitsu Tahara, Tomoyuki Shibata, Masakatsu Nakamura, Hiromi Yamashita, Daisuke Yoshioka, Ichiro Hirata, Tomiyasu Arisawa Source Type: journals

Neurofibromin physically interacts with the N-terminal domain of focal adhesion kinaseEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In this report, we show for the first time physical interaction between neurofibromin and focal adhesion kinase (FAK), the protein that localizes at focal adhesions. We show that neurofibromin associates with the N-terminal domain of FAK, and that the C-terminal domain of neurofibromin directly interacts with FAK. Confocal microscopy demonstrates colocalization of NF1 and FAK in the cytoplasm, perinuclear and nuclear regions inside the cells. Nf1+/+ MEF cells expressed less cell growth during serum deprivation conditions, and adhered less on collagen and fibronectin-treated plates than Nf1-/- MEF cells, associated with cha...
Source: Molecular Carcinogenesis - May 31, 2009 Category: Molecular Biology Authors: Frederick Kweh, Min Zheng, Elena Kurenova, Margaret Wallace, Vita Golubovskaya, William G. Cance Source Type: journals

Diallyl trisulfide-induced apoptosis in human cancer cells is linked to checkpoint kinase 1-mediated mitotic arrestEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
In conclusion, the results of the present study indicate that Chk1 dependence of DATS-induced mitotic arrest in human cancer cells is not influenced by the p53 status and cells arrested in mitosis upon DATS exposure are driven to apoptotic DNA fragmentation. © 2009 Wiley-Liss, Inc. (Source: Molecular Carcinogenesis)
Source: Molecular Carcinogenesis - May 21, 2009 Category: Molecular Biology Authors: Dong Xiao, Yan Zeng, Shivendra V. Singh Source Type: journals

The Ron receptor tyrosine kinase is not required for adenoma formation in ApcMin/+ miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
The Ron receptor tyrosine kinase is overexpressed in approximately half of all human colon cancers. Increased Ron expression positively correlates with tumor progression, and reduction of Ron levels in human colon adenocarcinoma cells reverses their tumorigenic properties. Nearly all colon tumors demonstrate loss of the adenomatous polyposis coli (APC) tumor suppressor, an early initiating event, subsequently leading to [beta]-catenin stabilization. To understand the role of Ron in early stage intestinal tumorigenesis, we generated Apc-mutant (ApcMin/+) mice with and without Ron signaling. Interestingly, we report here tha...
Source: Molecular Carcinogenesis - May 19, 2009 Category: Molecular Biology Authors: Sara E. Meyer, Susan E. Waltz, Kathleen H. Goss Source Type: journals

Specific IKK[beta] inhibitor IV blocks streptonigrin-induced NF-[kappa]B activity and potentiates its cytotoxic effect on cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Many anticancer agents activate NF-[kappa]B, which plays an important role in the survival of cancer cells. Inhibition of NF-[kappa]B activity may therefore potentiate the efficacy of anticancer agents. We found that a previously used anticancer agent Streptonigrin (SN) was also a potent NF-[kappa]B inducer. Using a specific IKK[beta] inhibitor IV (Podolin et al., J Pharmacol Exp Ther 2005; 312: 373-381), we revealed that the activation of NF-[kappa]B was mediated through DNA damage-induced activation of IKK complex. Furthermore, we demonstrated that SN-induced DNA damage was unrelated to reactive oxygen species but to the...
Source: Molecular Carcinogenesis - May 15, 2009 Category: Molecular Biology Authors: Maria Gavriil, Cheng-Chung Tsao, Sreekala Mandiyan, Kim Arndt, Robert Abraham, Yixian Zhang Source Type: journals

Urothelial overexpression of insulin-like growth factor-1 increases susceptibility to p-cresidine-induced bladder carcinogenesis in transgenic miceEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
To establish a role for insulin-like growth factor-1 (IGF-1) in bladder cancer susceptibility, we tested the effect of p-cresidine, a potent bladder carcinogen, in transgenic (TG) mice with human IGF-1 expression in the bladder driven by the bovine keratin 5 promoter (referred to as BK5.IGF-1 TG mice). Indomethacin was also tested to determine if the cyclooxygenase (COX) pathway is a target for bladder cancer prevention in this model. Thirty-three female BK5.IGF-1 TG mice and 29 female nontransgenic littermates were randomized to the following treatments: (1) AIN-76A diet; (2) AIN-76A diet with 0.5% p-cresidine; or (3) AIN...
Source: Molecular Carcinogenesis - May 7, 2009 Category: Molecular Biology Authors: Stephen D. Hursting, Susan N. Perkins, Jackie A. Lavigne, Linda Beltran, Diana C. Haines, Heather L. Hill, W. Gregory Alvord, J. Carl Barrett, John DiGiovanni Source Type: journals

Regulation of CDX2 expression in esophageal adenocarcinomaEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Reflux of acidic gastric contents and bile acids into the lower esophagus has been identified to have a central role in esophageal malignancy and is reported to upregulate caudal-related homologue 2 (CDX2), a regulatory gene involved in embryonic development and axial patterning of the alimentary tract. The aim of this study was to characterize the expression of CDX2 in a well-defined series of human esophageal tissues, comprising reflux-induced esophagitis, premalignant Barrett esophagus (BE), and primary esophageal adenocarcinoma (EADC). To explore potential molecular regulatory mechanisms, we also studied the expression...
Source: Molecular Carcinogenesis - May 4, 2009 Category: Molecular Biology Authors: Nadine Vaninetti, Lara Williams, Laurette Geldenhuys, Geoffrey A. Porter, Duane L. Guernsey, Alan G. Casson Source Type: journals

Cyclin D1b variant promotes cell invasiveness independent of binding to CDK4 in human bladder cancer cellsEmail this article to a colleague. Save this article to My Clippings. Discuss or comment on this article.
Alternative splicing in the cyclin D1 gene produces cyclin D1b variant which lacks a C-terminal region containing the threonine-286 (T286) phosphorylation site required for nuclear export. We have shown that the expression of the cyclin D1b variant is detected in about 60% of human bladder cancer tissues (15/26) and cell lines (3/5). To examine the role of the cyclin D1b variant in bladder carcinogenesis, we introduced wild-type cyclin D1a, cyclin D1b variant or mutant cyclin D1-T286A cDNAs into a human bladder cancer cell line, SBT991, in which cyclin D1b transcript was not expressed, and compared their oncogenic activiti...
Source: Molecular Carcinogenesis - May 4, 2009 Category: Molecular Biology Authors: Chul Jang Kim, Kayoko Nishi, Takahiro Isono, Yusuke Okuyama, Yukihiro Tambe, Yusaku Okada, Hirokazu Inoue Source Type: journals