Cellular signalling最新文献

{"title":"FAAP100:A biomarker based on pan-cancer analysis, promotes the progression of lung adenocarcinoma","authors":"Di Wu ,&nbsp;Min Gao ,&nbsp;Baochen Zhou ,&nbsp;Chunyang Zhu ,&nbsp;Yingxu Luo ,&nbsp;Fan Xia ,&nbsp;Xinran Wang ,&nbsp;Haiteng Liu ,&nbsp;Xin Zheng","doi":"10.1016/j.cellsig.2025.111950","DOIUrl":"10.1016/j.cellsig.2025.111950","url":null,"abstract":"<div><div>FAAP100 plays an essential role in DNA damage repair, with dysregulation associated with elevated cancer susceptibility. Nevertheless, comprehensive pan-cancer analyses examining FAAP100 prognostic significance, immune correlations, and epigenetic regulation remains unexplored. This study systematically characterized FAAP100 across 33 cancer types utilizing multi-omics data from TCGA, UALCAN, cBioPortal, TIMER2.0, and CPTAC. Analytical assessments included expression profiles, prognostic significance, and diagnostic utility, alongside associations with DNA methylation, immune cell infiltration, immune checkpoint gene expression, tumor mutational load (TMB), microsatellite instability (MSI), and drug resistance. Findings revealed significant FAAP100 upregulation across multiple cancer types, exhibiting inverse correlations to patient survival. Genomic characterization identified associations between FAAP100 overexpression and both copy number amplification and promoter hypomethylation. Immune profiling demonstrated robust correlations with immune cell infiltration levels and checkpoint molecule activity. Functional assays utilizing PC9 and H1299 cells indicated that FAAP100 enhances cellular proliferation and migration while inhibiting apoptosis processes. In vivo studies confirmed tumor growth suppression upon FAAP100 knockdown. Collectively, this multi-omics investigation identifies FAAP100 as a pan-cancer oncogene driver, highlighting its potential as both a prognostic biomarker and therapeutic target. The integrated analysis of expression patterns, epigenetic modifications, immune characteristics, and genomic alterations elucidates the mechanistic involvement of FAAP100 in tumor progression, providing a foundation for clinical application in precision oncology approaches..</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111950"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322206","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":"TYROBP overexpression alters macrophage phenotype and enhances pancreatic cancer stemness through STAT3 and PKM2 signaling","authors":"Dingwen Zhong ,&nbsp;Yonghui Liao ,&nbsp;Wenhui Chen ,&nbsp;Xianyu Huang ,&nbsp;Jiaxin Liu ,&nbsp;Xinsong Fu ,&nbsp;Zheng Wang","doi":"10.1016/j.cellsig.2025.111949","DOIUrl":"10.1016/j.cellsig.2025.111949","url":null,"abstract":"<div><h3>Background</h3><div>Pancreatic ductal adenocarcinoma (PDAC) is characterized by a complex tumor microenvironment (TME) that influences tumor progression and therapeutic responses. TYRO protein tyrosine kinase binding protein (TYROBP), a transmembrane polypeptide involved in immune cell signaling, has been implicated in PDAC and associated with M2 macrophage polarization.</div></div><div><h3>Methods</h3><div>We investigated the correlation between TYROBP expression and M2 macrophage infiltration in PDAC tissues using multiplex immunofluorescence staining. We also engineered TYROBP overexpression in SW1990 and Capan-1 pancreatic cancer cell lines to evaluate its impact on cell migration and macrophage polarization. Furthermore, we conducted co-culture experiments with SW1990 cells and THP-1 cells to explore the role of TYROBP in macrophage-mediated SW1990 cell proliferation and stemness. Nuclear translocation of STAT3 and PKM2 was assessed in TYROBP-overexpressing SW1990 cells, and the regulatory effects of STAT3 and PKM2 on CXCL8 expression were examined. Finally, molecular docking studies were performed to evaluate the binding of baicalein to STAT3, and in vivo studies assessed the inhibitory effects of baicalein on SW1990 cell proliferation.</div></div><div><h3>Results</h3><div>High TYROBP expression in PDAC tissues correlated with increased M2 macrophage infiltration, as indicated by elevated CD68 and CD206 levels. TYROBP overexpression promotes M2 macrophage polarization and glycolytic reprogramming via STAT3/PKM2, validated in vitro and in vivo. TYROBP overexpression also promoted the nuclear translocation of STAT3 and PKM2, enhancing glycolytic activity in SW1990 cells. STAT3 and PKM2 cooperated to regulate CXCL8 expression via direct binding to the CXCL8 promoter region. Molecular docking demonstrated baicalein's binding to STAT3, and in vivo studies showed that baicalein significantly inhibited SW1990 cell growth and modulated key signaling pathways.</div></div><div><h3>Conclusions</h3><div>Our study reveals that high TYROBP expression is associated with increased M2 macrophage infiltration in PDAC, promoting a pro-tumorigenic TME. TYROBP overexpression drives macrophage polarization towards the M2 phenotype, enhances glycolytic activity, and modulates key signaling pathways. Baicalein, targeting STAT3, shows potential as a therapeutic agent for PDAC by inhibiting cell proliferation and modulating the TME. These findings highlight TYROBP as a key regulator in PDAC progression and suggest potential therapeutic strategies targeting TYROBP and its associated pathways.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111949"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144322212","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":"GALNT6 dual regulates innate immunity STING signaling and PD-L1 expression to promote immune evasion in pancreatic ductal adenocarcinoma","authors":"Suli Chong ,&nbsp;Yang Liu ,&nbsp;Ziming Bian ,&nbsp;Dongxue Hu ,&nbsp;Shiqun Guo ,&nbsp;Chenfei Dong ,&nbsp;Jiayue Zeng ,&nbsp;Sairong Fan ,&nbsp;Xiaoming Chen","doi":"10.1016/j.cellsig.2025.111942","DOIUrl":"10.1016/j.cellsig.2025.111942","url":null,"abstract":"<div><div>Despite significant advancements in immunotherapy for cancer treatment, its effectiveness in pancreatic ductal adenocarcinoma (PDAC) remains disappointing, which is greatly due to the unique immunosuppressive microenvironment of PDAC. Here, we focus on the involvement of GALNT6 in immune evasion mechanisms in PDAC. Our results reveal a negative relationship between GALNT6 expression and immune cell infiltration in PDAC. Knockdown of GALNT6 enhances PDAC cells sensitivity to cytotoxic T cells and macrophages. Mechanistically, GALNT6-mediated glycosylation blocks the translocation of STING (stimulator of interferon genes) and accelerates its degradation in a cGAS-independent manner, leading to reduced levels of type I interferon (IFN-β) and CCL5 and CXCL10, thus promoting PDAC immune evasion by inhibiting cytotoxic CD8⁺ T cell and macrophage infiltration. Furthermore, GALNT6 stabilizes PD-L1 by blocking its ubiquitin-proteasome degradation, thereby promoting tumor immune evasion. Notably, the combination of an O-glycosylation inhibitor with PD-1/PD-L1 inhibitors synergistically enhances the anti-cancer immune response. In summary, these findings highlight GALNT6 as a critical player in immune evasion, and targeting GALNT6 could serve as a valuable approach to boost anti-tumor immunity in PDAC patients.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111942"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330900","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":"The role of FAK signaling in early placental development and trophoblast lineage specification in human pregnancy","authors":"Hong-Xiu Liang ,&nbsp;Cen Yi ,&nbsp;Si-Hui He ,&nbsp;Li-Yang Zhou ,&nbsp;Fang-Fang Li ,&nbsp;Jing Tang ,&nbsp;En-Xiang Chen ,&nbsp;Li-Juan Fu ,&nbsp;Ying-Xiong Wang ,&nbsp;You-Long Xie ,&nbsp;Yu-Bin Ding","doi":"10.1016/j.cellsig.2025.111946","DOIUrl":"10.1016/j.cellsig.2025.111946","url":null,"abstract":"<div><div>The placenta serves as a vital interface for fetal-maternal exchange, relying on trophoblast differentiation for development. This process involves cytotrophoblasts (CTBs) transitioning into syncytiotrophoblasts (STBs) and extravillous trophoblasts (EVTs), driving placental maturation. Focal adhesion kinase (FAK), a key cytoplasmic tyrosine kinase, regulates cellular processes such as proliferation, survival, and signaling. However, its role in trophoblast differentiation and metabolism remains unclear. Here, using human trophoblast stem cells (hTSCs) and trophoblast cell lines (BeWo, HTR8/SVneo), we investigated FAK signaling in trophoblast lineage differentiation. Inhibiting the FAK signaling pathway suppresses MAPK pathway activity, reduces glycolytic metabolism and impairs trophoblast syncytialization. Additionally, blocking FAK with the inhibitor Defactinib disrupts EVTs cytoskeleton and impairs migration, invasion, and differentiation potential. Notably, reduced FAK signaling is observed in patients with recurrent spontaneous abortion (RSA), suggesting a role in RSA pathogenesis. Our findings highlight FAK as a pivotal regulator of trophoblast lineage development, linking it to placental function and RSA. This study offers new insights into placental disorders and potential therapeutic targets.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111946"},"PeriodicalIF":4.4,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330899","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":"USP7-DDX5-FASN axis drives fatty acid metabolism and supports hepatocellular carcinoma progression","authors":"Jiawei Wang ,&nbsp;Lihua Zhou ,&nbsp;Yujia Pan ,&nbsp;Cai Li ,&nbsp;Shuxian Huang ,&nbsp;Zhaofang Yan ,&nbsp;Haipeng Wang ,&nbsp;Guangying Qi ,&nbsp;Jinfeng Gan","doi":"10.1016/j.cellsig.2025.111947","DOIUrl":"10.1016/j.cellsig.2025.111947","url":null,"abstract":"<div><div>Lipid metabolism plays a critical role in meeting the biosynthetic demands of rapidly proliferating tumor cells and is a major driver in the development of hepatocellular carcinoma (HCC). However, the precise molecular mechanisms underlying this process remain unclear. In this study, we identified DEAD box protein 5 (DDX5) as a key regulator of fatty acid synthesis in HCC. Analysis of multiple HCC cohorts revealed a marked elevation in DDX5 expression, which is closely correlated with poorer clinical outcomes. Functional studies demonstrated that DDX5 facilitates HCC cell proliferation, enhances colony formation, and promotes fatty acid synthesis through the upregulation of fatty acid synthetase (FASN). In vivo studies showed that inhibition of DDX5 effectively suppressed tumor growth. Further investigation identified an interaction between DDX5 and ubiquitin-specific peptidase 7 (USP7), whereby USP7 stabilizes DDX5 by removing ubiquitin chains through deubiquitination. Collectively, these findings highlight the USP7-DDX5-FASN axis as a critical regulator of fatty acid metabolism in HCC progression, offering potential avenues for therapeutic intervention.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111947"},"PeriodicalIF":4.4,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144330898","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":"Activation of STING pathway by mitochondrial fission negatively regulates adipogenic differentiation of 3 T3-L1 cells.","authors":"Kai Ma, Haoxuan Sun, Xiaoyun Wu, Jinping Quan, Rong Tang, Weiwei Liu, Toshihiko Hayashi, Kazunori Mizuno, Shunji Hattori, Hitomi Fujisaki, Takashi Ikejima","doi":"10.1016/j.cellsig.2025.111948","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111948","url":null,"abstract":"<p><p>Adipocyte hyperplasia refers to the increase in the number of adipocytes, whereas adipocyte hypertrophy pertains to the enlargement of individual adipocytes resulting from the accumulation of lipid droplets. In this study, we found that activation of the STING signalling pathway occurs during adipogenic differentiation of 3 T3-L1 preadipocytes. Interestingly, inhibiting the STING pathway by using STING antagonist H151 or siRNA targeting STING promotes adipocyte differentiation and increases adipocyte numbers, while activation of STING inhibits adipogenic differentiation. Silencing the STING canonical downstream IRF3, or inhibiting the proton channel activity of STING enhances adipogenic differentiation, confirming the negative modulation of adipogenic differentiation by STING. In vivo, intraperitoneal injection of H151 into mice with a high-fat diet further enhances the adipocyte hyperplasia, as shown by the increased volume of adipose tissues, but consistent sizes of adipocytes. During the adipogenic differentiation of 3 T3-L1 cells, DRP1-mediated mitochondrial fission is enhanced, and causes mitochondrial DNA leakage, which in turn activates the STING pathway. However, inhibition of mitochondrial fission represses adipogenic differentiation of 3 T3-L1 cells in spite of the down-regulation of STING pathway. Therefore, our results indicate that adipogenic differentiation is associated with DRP1-induced mitochondrial fission. However, the leakage of mitochondrial DNA caused by DRP1-induced mitochondrial fission activates the STING signalling pathway, which negatively regulates adipogenic differentiation. Tissue specific reduction of DRP1-associated mitochondrial fission or STING enhancement might be new strategies for the therapy of obesity-associated diseases.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111948"},"PeriodicalIF":4.4,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144324550","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":"TNALP promotes epithelial oxidative stress and fibrosis via SIRT3-dependent mechanisms in tracheal injury","authors":"Zhiqiang Liu ,&nbsp;Hailang Peng ,&nbsp;Mingyu Peng ,&nbsp;Jiaxin Liao ,&nbsp;Bin Liu ,&nbsp;Rongjuan Zhuang ,&nbsp;Hongwei Yang ,&nbsp;Li Xu ,&nbsp;Yishi Li ,&nbsp;Lei Gao ,&nbsp;Shuliang Guo","doi":"10.1016/j.cellsig.2025.111943","DOIUrl":"10.1016/j.cellsig.2025.111943","url":null,"abstract":"<div><div>Benign tracheal stenosis (BTS) remains a clinical challenge due to high postoperative restenosis rates and the absence of effective pharmacological treatments. Although fibrosis has traditionally been attributed to fibroblast activation, epithelial injury is increasingly recognized as an early initiating event. This study identified tissue-nonspecific alkaline phosphatase (TNALP) as a key mediator of epithelial damage and fibrotic progression in BTS. Analyses of patient specimens, animal models, and cultured epithelial cells revealed that TNALP suppressed SIRT3 expression level, a mitochondrial deacetylase that can regulate oxidative stress and apoptosis. Pharmacological inhibition of TNALP with tetramisole restored SIRT3 expression level, attenuated oxidative damage, reduced epithelial cell death, and mitigated tissue fibrosis. These preclinical findings highlight TNALP as a potential therapeutic target and support further investigation into the repurposing of TNALP inhibitors as antifibrotic agents to reduce restenosis following tracheal surgery.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111943"},"PeriodicalIF":4.4,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307675","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":"miRNA-548d-3p represses non-small cell lung cancer growth by perturbing DDX5-mediated pyroptosis through JAK2/STAT3 signaling","authors":"Liyu Liu ,&nbsp;Qinglin Liu ,&nbsp;Zhining Wu ,&nbsp;Jiao Wu ,&nbsp;Xiaoyan Chen ,&nbsp;Bocheng Zhang ,&nbsp;Xiao Pang ,&nbsp;Shixuan Liang ,&nbsp;Ying Long ,&nbsp;Ying Liu","doi":"10.1016/j.cellsig.2025.111945","DOIUrl":"10.1016/j.cellsig.2025.111945","url":null,"abstract":"<div><h3>Background</h3><div>The function of microRNAs (miRNAs) in tumor development has been extensively characterized. Pyroptosis is a kind of programmed death, which can effectively hinder cancer development. However, there is still a large gap in the function of miRNAs in NSCLC pyroptosis.</div></div><div><h3>Methods</h3><div>The pyroptosis-related differentially expressed miRNAs and their promising targets in NSCLC were analyzed using bioinformatic analyses. The effects of miR-548d-3p on cell proliferation, pyroptosis and tumor growth were verified in vivo and in vitro. The expression of pyroptosis-related factors was examined in cells and xenografted tumors. Additionally, the molecular interaction was assessed by using Co-IP and dual-luciferase reporter gene assays.</div></div><div><h3>Results</h3><div>We found that miR-548d-3p was poorly expressed in NSCLC in public datasets and an independent cohort of 48 NSCLC patients. Low miR-548d-3p expression was positively associated with pathologic T stage and poor prognosis of NSCLC patients. Transfection of miR-548d-3p mimics significantly decreased the cell viability of NSCLC cells, partly attributing to the increase in the proportion of pyroptotic cells. These changes were accompanied by a rise in the protein abundance of NLRP3, ASC, cleaved Caspase-1 and GSDMD-N and release of IL-1β and IL-18. Integrating bioinformatic, expressional and experimental analyses, we predicted and validated DDX5 as the direct target of miR-548d-3p. Furthermore, we demonstrated that miR-548d-3p/DDX5 axis regulated pyroptosis via the Phosphorylated JAK2/STAT3-mediated NLRP3/Caspase-1/GSDMD pathway in vitro and in vivo.</div></div><div><h3>Conclusion</h3><div>Our study revealed that miR-548d-3p/DDX5 promoted pyroptosis in NSCLC by promoting the JAK2/STAT3/NLRP3/Caspase-1/GSDMD pathway, indicating the promising effect of miR-548d-3p in NSCLC treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111945"},"PeriodicalIF":4.4,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315997","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":"Identification of lactylation-related hub genes as novel therapeutic and diagnostic targets for thoracic aortic dissection","authors":"Jinxing Peng ,&nbsp;Zhuohang Jiang ,&nbsp;Jiayu Song ,&nbsp;Jinze Chen ,&nbsp;Ziyun Fu ,&nbsp;Huizhe Zhang ,&nbsp;Jianfan Zhen ,&nbsp;Muhetaijiang Tuerdi ,&nbsp;Mingyang Luo ,&nbsp;Jinlin Wu ,&nbsp;Tucheng Sun","doi":"10.1016/j.cellsig.2025.111944","DOIUrl":"10.1016/j.cellsig.2025.111944","url":null,"abstract":"<div><h3>Background</h3><div>Thoracic aortic dissection (TAD) is a life-threatening cardiovascular disease with high mortality rates. Although lactylation has garnered increasing attention, its role in TAD remains poorly understood.</div></div><div><h3>Methods</h3><div>Lactylation-related genes (LRGs) were obtained from the MsigDB database. Lactylation-related hub genes (LRHGs) were identified by intersecting LRGs with differentially expressed genes and WGCNA results. Lactylation was assessed in a β-aminopropionitrile (BAPN)-induced mouse model and human aortic tissues. Two single-cell RNA sequencing (scRNA-seq) from the GEO database were utilized to evaluate lactylation patterns across cell populations and intercellular communication networks. Biomarkers were evaluated using receiver operating characteristic (ROC) analysis.</div></div><div><h3>Results</h3><div>Elevated lactylation levels were observed in both TAD tissues and synthetic phenotype vascular smooth muscle cells. Through integrated analysis, we identified 12 LRHGs, which includes LDHA. In the BAPN-induced mouse model, LDHA inhibitors (Oxamate and FX11) significantly reduced mortality rates and decreased aortic lactate levels and protein lactylation. ScRNA-seq analytic results revealed that monocytes and macrophages exhibited the highest lactylation activity, which likely enhanced their inflammatory pathways and intercellular communication. ROC analysis showed the lowest AUC of 12 LRHGs is 0.8893.</div></div><div><h3>Conclusions</h3><div>This study highlights the critical role of lactylation-related hub genes in TAD, identifying potential therapeutic targets and diagnostic biomarkers, which provides novel insights into the molecular mechanisms underlying TAD.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"134 ","pages":"Article 111944"},"PeriodicalIF":4.4,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144315981","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":"Corrigendum to \"O-GlcNAcylated c-Jun antagonizes ferroptosis via inhibiting GSH synthesis in liver cancer\" [Cellular Signalling, 2019 Nov:63:109384. doi:10.1016/j.cellsig.2019.109384].","authors":"Yan Chen, Guoqing Zhu, Ya Liu, Qi Wu, Xiao Zhang, Zhixuan Bian, Yue Zhang, Qiuhui Pan, Fenyong Sun","doi":"10.1016/j.cellsig.2025.111915","DOIUrl":"https://doi.org/10.1016/j.cellsig.2025.111915","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"111915"},"PeriodicalIF":4.4,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301204","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}