Gurdeep Marwarha, Kate Claycombe, Jared Schommer, David Collins, Othman Ghribi
{"title":"Retraction notice to \"Palmitate-induced Endoplasmic Reticulum stress and subsequent C/EBPα Homologous Protein activation attenuates leptin and Insulin-like growth factor 1 expression in the brain\" [Cellular Signalling 28 (2016) 1789-1805].","authors":"Gurdeep Marwarha, Kate Claycombe, Jared Schommer, David Collins, Othman Ghribi","doi":"10.1016/j.cellsig.2026.112872","DOIUrl":"10.1016/j.cellsig.2026.112872","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112872"},"PeriodicalIF":4.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Expression of Concern: \"Musashi-2 binds with Fbxo6 to induce Rnaset2 ubiquitination and chemokine signaling pathway during vascular smooth muscle cell phenotypic switch in atherosclerosis\" [Cellular Signalling, Volume 111, November 2023, 110869].","authors":"","doi":"10.1016/j.cellsig.2026.112901","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112901","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112901"},"PeriodicalIF":4.7,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Retraction notice to \"Endoplasmic reticulum stress-induced CHOP activation mediates the down-regulation of leptin in human neuroblastoma SH-SY5Y cells treated with the oxysterol 27-hydroxycholesterol\" [Cellular Signalling 24 (2012) 484-492].","authors":"Gurdeep Marwarha, Bhanu Dasari, Othman Ghribi","doi":"10.1016/j.cellsig.2026.112873","DOIUrl":"10.1016/j.cellsig.2026.112873","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112873"},"PeriodicalIF":4.7,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148988065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jian Yuan, Yangxian Xu, Yizhe Diao, Tao Ding, Guorong Yuan
{"title":"Rg3 suppresses gastric cancer progression via TFEB-mediated lysosomal autophagy pathway.","authors":"Jian Yuan, Yangxian Xu, Yizhe Diao, Tao Ding, Guorong Yuan","doi":"10.1016/j.cellsig.2026.112892","DOIUrl":"10.1016/j.cellsig.2026.112892","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) ranks among the most prevalent malignant tumors globally, characterized by elevated incidence and mortality rates. As a natural active component isolated from Panax ginseng, Rg3 has demonstrated anti-tumor activity across multiple malignancies. Nevertheless, its specific functions and underlying molecular mechanisms in GC remain incompletely elucidated.</p><p><strong>Methods: </strong>Rg3 exerted effects in viability, proliferative capacity, apoptotic progression, and autophagy-associated protein expression in AGS cells, evaluated via CCK-8 assay, colony formation, EdU staining, flow cytometry, and Western blot. To investigate the direct interaction between Rg3 and TFEB, as well as the mechanism by which Rg3 modulated apoptosis via lysosomal autophagy, the molecular docking, CETSA, immunofluorescence, mRFP-GFP-LC3 dual-labeling system, LysoTracker/Magic Red staining, and gene knockdown/overexpression approaches were employed. The expression of AKT/mTOR pathway-related proteins was analyzed by Western blot. A nude mouse xenograft tumor model was established to monitor tumor development, while H&E staining and IHC were employed to dissect histopathological alterations and the expression of pivotal proteins.</p><p><strong>Results: </strong>Rg3 attenuated the proliferation of AGS cells in a concentration-dependent manner, induced apoptosis, and inhibited the AKT/mTOR pathway. Mechanistic investigations unveiled that Rg3, on one hand, reduced TFEB phosphorylation by inhibiting the AKT/mTOR pathway, thereby driving TFEB nuclear translocation; on the other hand, it bound to TFEB to enhance its protein stability, maintained the activated state of TFEB, and upregulated TFEB protein expression, consequently activating the lysosomal autophagy pathway. TFEB knockdown reversed Rg3-mediated autophagy activation, apoptosis induction, and development inhibition, whereas TFEB overexpression recapitulated these effects, which were abrogated by the autophagy inhibitor chloroquine. In vivo experiments further verified that Rg3 prominently suppressed xenograft tumor development, concurrent with upregulated TFEB and LC3B expressions, downregulated Ki67, and elevated Bax levels in tumor tissues.</p><p><strong>Conclusion: </strong>Rg3 upregulates and activates TFEB, thereby triggering the lysosomal autophagy pathway, which ultimately induces GC cell apoptosis and suppresses tumor progression.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112892"},"PeriodicalIF":4.7,"publicationDate":"2026-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Daoyuan Li, Jun Jiang, Ming Ge, Mengting He, Yinmao Yang, Min Liu, Yuchong Feng, Yiming Wu, Shangkun Ou
{"title":"Inhibition of YAP signaling suppresses fibrosis and posterior capsular opacification in preclinical models of cataract surgery.","authors":"Daoyuan Li, Jun Jiang, Ming Ge, Mengting He, Yinmao Yang, Min Liu, Yuchong Feng, Yiming Wu, Shangkun Ou","doi":"10.1016/j.cellsig.2026.112889","DOIUrl":"10.1016/j.cellsig.2026.112889","url":null,"abstract":"<p><strong>Purpose: </strong>A frequent fibrotic sequela following cataract intervention is posterior capsular opacification (PCO), which is primarily triggered by lens epithelial cells (LECs) undergoing epithelial-mesenchymal transition (EMT). The objective of this research was to examine how yes-associated protein (YAP) modulates EMT in LECs and to determine the contribution of connective tissue growth factor (CTGF) to this regulatory axis.</p><p><strong>Methods: </strong>A simulated cataract surgery model was established in C57BL/6 mice to examine YAP expression during postoperative EMT in lens epithelium. EMT was induced in human SRA01/04 LECs and mouse primary lens epithelial explants using transforming growth factor-β1 (TGF-β1). YAP expression and activity were modulated by lentiviral-mediated knockdown or overexpression and pharmacological inhibition using verteporfin. To evaluate the expression of YAP-related target genes and EMT markers, techniques including real-time PCR, Western blot, and immunofluorescence were employed. The role of CTGF was evaluated using a neutralizing antibody.</p><p><strong>Results: </strong>YAP expression was increased in LECs following simulated cataract surgery and throughout the process of TGF-β1-mediated EMT within cultured cells. Suppression of YAP expression or activity significantly attenuated EMT, characterized by the downregulation of Fibronectin and α-SMA alongside the maintenance of epithelial markers. Conversely, YAP overexpression promoted EMT-associated molecular changes. Neutralization of CTGF partially reversed YAP-induced EMT, indicating CTGF contributes to YAP-dependent EMT regulation.</p><p><strong>Conclusions: </strong>The progression of EMT in LECs is driven by YAP activation, a process that occurs, to a certain extent, via the enhancement of CTGF expression. Targeting YAP signaling may represent a potential therapeutic strategy for preventing EMT-driven PCO following cataract surgery.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112889"},"PeriodicalIF":4.7,"publicationDate":"2026-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}