E2F8-CENPL pathway contributes to homologous recombination repair and chemoresistance in breast cancer
Cell Signal. 2024 Mar 22:111151. doi: 10.1016/j.cellsig.2024.111151. Online ahead of print.ABSTRACTChemoresistance poses a significant obstacle to the treatment of breast cancer patients. The increased capacity of DNA damage repair is one of the mechanisms underlying chemoresistance. Bioinformatic analyses showed that E2F8 was associated with cell cycle progression and homologous recombination (HR) repair of DNA double-strand breaks (DSBs) in breast cancer. E2F8 knockdown suppressed cell growth and attenuated HR repair. Accordingly, E2F8 knockdown sensitized cancer cells to Adriamycin and Cisplatin. Centromere protein L (C...
Source: Cellular Signalling - March 24, 2024 Category: Cytology Authors: Shan Wang Yuhong Xia Yu Sun Wei Wang Lianfeng Shan Zhongbo Zhang Chenghai Zhao Source Type: research

Deciphering the role of glycosaminoglycans in GPCR signaling
Cell Signal. 2024 Mar 22:111149. doi: 10.1016/j.cellsig.2024.111149. Online ahead of print.ABSTRACTG protein-coupled receptors (GPCR) and glycosaminoglycans (GAGs) are two essential components of the cell surface that regulate physiological processes in the body. GPCRs are the most extensive family of transmembrane receptors that control cellular responses to extracellular stimuli, while GAGs are polysaccharides that contribute to the function of the extracellular matrix (ECM). Due to their proximity to the plasma membrane, GAGs participate in signal transduction by interacting with various extracellular molecules and cell...
Source: Cellular Signalling - March 24, 2024 Category: Cytology Authors: Sofya Savransky Alex D White Jean-Pierre Vilardaga Source Type: research

E2F8-CENPL pathway contributes to homologous recombination repair and chemoresistance in breast cancer
Cell Signal. 2024 Mar 22:111151. doi: 10.1016/j.cellsig.2024.111151. Online ahead of print.ABSTRACTChemoresistance poses a significant obstacle to the treatment of breast cancer patients. The increased capacity of DNA damage repair is one of the mechanisms underlying chemoresistance. Bioinformatic analyses showed that E2F8 was associated with cell cycle progression and homologous recombination (HR) repair of DNA double-strand breaks (DSBs) in breast cancer. E2F8 knockdown suppressed cell growth and attenuated HR repair. Accordingly, E2F8 knockdown sensitized cancer cells to Adriamycin and Cisplatin. Centromere protein L (C...
Source: Cellular Signalling - March 24, 2024 Category: Cytology Authors: Shan Wang Yuhong Xia Yu Sun Wei Wang Lianfeng Shan Zhongbo Zhang Chenghai Zhao Source Type: research

Deciphering the role of glycosaminoglycans in GPCR signaling
Cell Signal. 2024 Mar 22:111149. doi: 10.1016/j.cellsig.2024.111149. Online ahead of print.ABSTRACTG protein-coupled receptors (GPCR) and glycosaminoglycans (GAGs) are two essential components of the cell surface that regulate physiological processes in the body. GPCRs are the most extensive family of transmembrane receptors that control cellular responses to extracellular stimuli, while GAGs are polysaccharides that contribute to the function of the extracellular matrix (ECM). Due to their proximity to the plasma membrane, GAGs participate in signal transduction by interacting with various extracellular molecules and cell...
Source: Cellular Signalling - March 24, 2024 Category: Cytology Authors: Sofya Savransky Alex D White Jean-Pierre Vilardaga Source Type: research

E3 ubiquitin ligase CHIP interacts with transferrin receptor 1 for degradation and promotes cell proliferation through inhibiting ferroptosis in hepatocellular carcinoma
Cell Signal. 2024 Mar 21:111148. doi: 10.1016/j.cellsig.2024.111148. Online ahead of print.ABSTRACTHepatocellular carcinoma (HCC) is the major form of liver malignancy with high incidence and mortality. Identifying novel biomarkers and understanding regulatory mechanisms underlying the development and progression of HCC are critical for improving diagnosis, treatment and patient outcomes. Carboxyl terminus of Hsc-70-interacting protein (CHIP) is a well-described U-box-type E3 ubiquitin ligase which promotes the ubiquitination and degradation of numerous tumor-associated proteins. Recent studies have shown that CHIP can pla...
Source: Cellular Signalling - March 23, 2024 Category: Cytology Authors: Miaomiao Shao Kangwei Qi Lanxin Wang Xiaoxuan Yu Qingyu Zhang Long Yu Lan Wang Caiting Yang Lu Fan Source Type: research

E3 ubiquitin ligase CHIP interacts with transferrin receptor 1 for degradation and promotes cell proliferation through inhibiting ferroptosis in hepatocellular carcinoma
Cell Signal. 2024 Mar 21:111148. doi: 10.1016/j.cellsig.2024.111148. Online ahead of print.ABSTRACTHepatocellular carcinoma (HCC) is the major form of liver malignancy with high incidence and mortality. Identifying novel biomarkers and understanding regulatory mechanisms underlying the development and progression of HCC are critical for improving diagnosis, treatment and patient outcomes. Carboxyl terminus of Hsc-70-interacting protein (CHIP) is a well-described U-box-type E3 ubiquitin ligase which promotes the ubiquitination and degradation of numerous tumor-associated proteins. Recent studies have shown that CHIP can pla...
Source: Cellular Signalling - March 23, 2024 Category: Cytology Authors: Miaomiao Shao Kangwei Qi Lanxin Wang Xiaoxuan Yu Qingyu Zhang Long Yu Lan Wang Caiting Yang Lu Fan Source Type: research

Unraveling the mechanism in l-Caldesmon regulating the osteogenic differentiation of PDLSCs: An innovative perspective
Cell Signal. 2024 Mar 19:111147. doi: 10.1016/j.cellsig.2024.111147. Online ahead of print.ABSTRACTMaxillofacial bone defect is one of the common symptoms in maxillofacial, which affects the function and aesthetics of maxillofacial region. Periodontal ligament stem cells (PDLSCs) are extensively used in bone tissue engineering. The mechanism that regulates the osteogenic differentiation of PDLSCs remains not fully elucidated. Previous studies demonstrated that l-Caldesmon (l-Cad, or Cald1) might be involved in the osteogenic differentiation of PDLSCs. Here, the mechanism by which Cald1 regulates the osteogenic differentiat...
Source: Cellular Signalling - March 21, 2024 Category: Cytology Authors: Yuejia Li Ziyi Mei Pingmeng Deng Sha Zhou Aizhuo Qian Xiya Zhang Jie Li Source Type: research

Unraveling the mechanism in l-Caldesmon regulating the osteogenic differentiation of PDLSCs: An innovative perspective
Cell Signal. 2024 Mar 19:111147. doi: 10.1016/j.cellsig.2024.111147. Online ahead of print.ABSTRACTMaxillofacial bone defect is one of the common symptoms in maxillofacial, which affects the function and aesthetics of maxillofacial region. Periodontal ligament stem cells (PDLSCs) are extensively used in bone tissue engineering. The mechanism that regulates the osteogenic differentiation of PDLSCs remains not fully elucidated. Previous studies demonstrated that l-Caldesmon (l-Cad, or Cald1) might be involved in the osteogenic differentiation of PDLSCs. Here, the mechanism by which Cald1 regulates the osteogenic differentiat...
Source: Cellular Signalling - March 21, 2024 Category: Cytology Authors: Yuejia Li Ziyi Mei Pingmeng Deng Sha Zhou Aizhuo Qian Xiya Zhang Jie Li Source Type: research

MZB1 regulates cellular proliferation, mitochondrial dysfunction, and inflammation and targets the PI3K-Akt signaling pathway in acute pancreatitis
CONCLUSIONS: AP cells and tissues exhibited markedly elevated levels of MZB1 expression compared to their healthy counterparts. MZB1 overexpression promoted proliferation and supressed apoptosis, mitochondrial dysfunction, and inflammation in pancreatic cells through the positive regulation of the PI3K-Akt signaling pathway.PMID:38508349 | DOI:10.1016/j.cellsig.2024.111143 (Source: Cellular Signalling)
Source: Cellular Signalling - March 20, 2024 Category: Cytology Authors: Mengtao Xu Yong Feng Xuelian Xiang Li Liu Guodu Tang Source Type: research

The PIEZO1/miR-155-5p/GDF6/SMAD2/3 signaling axis is involved in inducing the occurrence and progression of osteoarthritis under excessive mechanical stress
CONCLUSION: GDF6 overexpression or miR-155-5p inhibition could attenuate overloading-induced chondrocyte senescence and OA through the PIEZO1-miR-155-5p-GDF6-SMAD2/3 signaling pathway. Our study provides a new therapeutic target for the treatment of overloading-induced OA.PMID:38508350 | DOI:10.1016/j.cellsig.2024.111142 (Source: Cellular Signalling)
Source: Cellular Signalling - March 20, 2024 Category: Cytology Authors: Chaoren Qin Yan Feng Zhaowei Yin Changjiang Wang Rui Yin Yang Li Kai Chen Tianqi Tao Kaibin Zhang Yiqiu Jiang Jianchao Gui Source Type: research

MZB1 regulates cellular proliferation, mitochondrial dysfunction, and inflammation and targets the PI3K-Akt signaling pathway in acute pancreatitis
CONCLUSIONS: AP cells and tissues exhibited markedly elevated levels of MZB1 expression compared to their healthy counterparts. MZB1 overexpression promoted proliferation and supressed apoptosis, mitochondrial dysfunction, and inflammation in pancreatic cells through the positive regulation of the PI3K-Akt signaling pathway.PMID:38508349 | DOI:10.1016/j.cellsig.2024.111143 (Source: Cellular Signalling)
Source: Cellular Signalling - March 20, 2024 Category: Cytology Authors: Mengtao Xu Yong Feng Xuelian Xiang Li Liu Guodu Tang Source Type: research

The PIEZO1/miR-155-5p/GDF6/SMAD2/3 signaling axis is involved in inducing the occurrence and progression of osteoarthritis under excessive mechanical stress
CONCLUSION: GDF6 overexpression or miR-155-5p inhibition could attenuate overloading-induced chondrocyte senescence and OA through the PIEZO1-miR-155-5p-GDF6-SMAD2/3 signaling pathway. Our study provides a new therapeutic target for the treatment of overloading-induced OA.PMID:38508350 | DOI:10.1016/j.cellsig.2024.111142 (Source: Cellular Signalling)
Source: Cellular Signalling - March 20, 2024 Category: Cytology Authors: Chaoren Qin Yan Feng Zhaowei Yin Changjiang Wang Rui Yin Yang Li Kai Chen Tianqi Tao Kaibin Zhang Yiqiu Jiang Jianchao Gui Source Type: research

Microglial uptake of hADSCs-Exo mitigates neuroinflammation in ICH
This study aims to investigate the role of hADSCs-Exo in ICH and its underlying mechanism involving miRNA-mediated regulation of formyl peptide receptor 1 (FPR1). Flow cytometry was used to identify hADSCs and extract exosomes. Transmission electron microscopy and Western blot were performed to confirm the characteristics of the exosomes. In vitro experiments were conducted to explore the uptake of hADSCs-Exo by microglia cells and their impact on inflammatory responses. In vivo, an ICH mouse model was established, and the therapeutic effects of hADSCs-Exo were evaluated through neurological function scoring, histological ...
Source: Cellular Signalling - March 18, 2024 Category: Cytology Authors: Lanqing Zhao Jinwei Li Source Type: research

Microglial uptake of hADSCs-Exo mitigates neuroinflammation in ICH
This study aims to investigate the role of hADSCs-Exo in ICH and its underlying mechanism involving miRNA-mediated regulation of formyl peptide receptor 1 (FPR1). Flow cytometry was used to identify hADSCs and extract exosomes. Transmission electron microscopy and Western blot were performed to confirm the characteristics of the exosomes. In vitro experiments were conducted to explore the uptake of hADSCs-Exo by microglia cells and their impact on inflammatory responses. In vivo, an ICH mouse model was established, and the therapeutic effects of hADSCs-Exo were evaluated through neurological function scoring, histological ...
Source: Cellular Signalling - March 18, 2024 Category: Cytology Authors: Lanqing Zhao Jinwei Li Source Type: research

WDR4 promotes HCC pathogenesis through N < sup > 7 < /sup > -methylguanosine by regulating and interacting with METTL1
CONCLUSIONS: WDR4 may contribute to HCC pathogenesis by interacting with and regulating the expression of METTL1 to synergistically modulate the m7G modification of target mRNAs in tumor cells.PMID:38493882 | DOI:10.1016/j.cellsig.2024.111145 (Source: Cellular Signalling)
Source: Cellular Signalling - March 17, 2024 Category: Cytology Authors: Rui Dong Chuanxu Wang Bo Tang Yayu Cheng Xuehui Peng Xiaomin Yang Bing Ni Jing Li Source Type: research