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Long noncoding RNA H19 in liver development and disease. 长链非编码RNA H19在肝脏发育和疾病中的作用。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-05 DOI: 10.1016/j.cellsig.2026.112413
Diego Elias Montoya-Durango, Leila Gobejishvili

Liver disease is a global health problem responsible for more than two million deaths annually. Metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) are major contributors to chronic liver disease-related morbidity and mortality. Factors like diet and alcohol consumption have become key drivers of liver pathologies including steatosis, fibrosis/cirrhosis, and hepatocellular carcinoma. To date very few treatments are available, hence there is a critical need for the development of novel therapies to slow down the development/progression of liver damage. The long non-coding RNA H19 gene, H19, is an imprinted gene normally expressed from the maternally inherited chromosome and epigenetically silenced in the paternal chromosome. At the embryo stage H19 controls genome-wide methylation, directs the methylation of the imprinted gene network, and regulates organ size. In the livers of neonates, H19 is important for organ maturation but remains silent in the mature organ. H19 re-expression in the adult liver drives de novo lipogenesis and fibrosis and maintains a proliferative state in tumor cells. The complexity of H19 functions in the liver is reflected in its interaction and regulation of a growing number of proteins, and coding and non-coding RNAs involved in metabolism, pro-fibrotic gene networks, cell cycle progression, and chromatin regulation. This review summarizes the findings related to the role of H19 in liver development and in diseases such as fatty liver, fibrosis, and hepatocellular carcinoma.

{"title":"Long noncoding RNA H19 in liver development and disease.","authors":"Diego Elias Montoya-Durango, Leila Gobejishvili","doi":"10.1016/j.cellsig.2026.112413","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112413","url":null,"abstract":"<p><p>Liver disease is a global health problem responsible for more than two million deaths annually. Metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) are major contributors to chronic liver disease-related morbidity and mortality. Factors like diet and alcohol consumption have become key drivers of liver pathologies including steatosis, fibrosis/cirrhosis, and hepatocellular carcinoma. To date very few treatments are available, hence there is a critical need for the development of novel therapies to slow down the development/progression of liver damage. The long non-coding RNA H19 gene, H19, is an imprinted gene normally expressed from the maternally inherited chromosome and epigenetically silenced in the paternal chromosome. At the embryo stage H19 controls genome-wide methylation, directs the methylation of the imprinted gene network, and regulates organ size. In the livers of neonates, H19 is important for organ maturation but remains silent in the mature organ. H19 re-expression in the adult liver drives de novo lipogenesis and fibrosis and maintains a proliferative state in tumor cells. The complexity of H19 functions in the liver is reflected in its interaction and regulation of a growing number of proteins, and coding and non-coding RNAs involved in metabolism, pro-fibrotic gene networks, cell cycle progression, and chromatin regulation. This review summarizes the findings related to the role of H19 in liver development and in diseases such as fatty liver, fibrosis, and hepatocellular carcinoma.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112413"},"PeriodicalIF":3.7,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137208","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}
引用次数: 0
Alpha-fetoprotein acts as a key regulator of cancer stemness in hepatocellular carcinoma via PI3K/Akt pathway 甲胎蛋白通过PI3K/Akt通路在肝细胞癌中起关键调控作用
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-05 DOI: 10.1016/j.cellsig.2026.112401
Gulijiamali Kahaer , Sirun Pan , Wenchen Xie, Yue Li, Chengcheng Yang, Xin Zhang, Han Wang, Yan Lu
Alpha-fetoprotein (AFP) is a well-established diagnostic biomarker for hepatocellular carcinoma (HCC), yet its functional role in tumor progression extends far beyond serological detection. Specifically, its ability to regulate cancer stemness, a key driver of therapy resistance and recurrence, remains largely unexplored. Here, we demonstrate that AFP is a critical functional regulator of cancer stem-like cells (CSC) in HCC. In this study, we employed CRISPR/Cas9-mediated gene editing to generate AFP-knockout models in Huh7 and PLC/PRF/5 cell lines, enabling a systematic investigation of AFP's oncogenic functions. Comparative analyses demonstrated that AFP ablation markedly reduced tumorigenic potential in vivo, accompanied by downregulation of stemness markers (EPCAM and CD44) and inhibition of PI3K/Akt signaling. Mechanistic studies further identified the PI3K/Akt pathway as critical for AFP-mediated maintenance of cancer stem cell properties. Collectively, our findings provide direct evidence that AFP-driven stemness contributes functionally to HCC progression, establishing AFP as a molecular regulator rather than merely a diagnostic marker. This study elucidates a novel AFP-PI3K/Akt-stemness axis in HCC pathogenesis and highlights potential therapeutic targets for stemness-directed interventions in AFP-positive HCC.
{"title":"Alpha-fetoprotein acts as a key regulator of cancer stemness in hepatocellular carcinoma via PI3K/Akt pathway","authors":"Gulijiamali Kahaer ,&nbsp;Sirun Pan ,&nbsp;Wenchen Xie,&nbsp;Yue Li,&nbsp;Chengcheng Yang,&nbsp;Xin Zhang,&nbsp;Han Wang,&nbsp;Yan Lu","doi":"10.1016/j.cellsig.2026.112401","DOIUrl":"10.1016/j.cellsig.2026.112401","url":null,"abstract":"<div><div>Alpha-fetoprotein (AFP) is a well-established diagnostic biomarker for hepatocellular carcinoma (HCC), yet its functional role in tumor progression extends far beyond serological detection. Specifically, its ability to regulate cancer stemness, a key driver of therapy resistance and recurrence, remains largely unexplored. Here, we demonstrate that AFP is a critical functional regulator of cancer stem-like cells (CSC) in HCC. In this study, we employed CRISPR/Cas9-mediated gene editing to generate AFP-knockout models in Huh7 and PLC/PRF/5 cell lines, enabling a systematic investigation of AFP's oncogenic functions. Comparative analyses demonstrated that AFP ablation markedly reduced tumorigenic potential in vivo, accompanied by downregulation of stemness markers (EPCAM and CD44) and inhibition of PI3K/Akt signaling. Mechanistic studies further identified the PI3K/Akt pathway as critical for AFP-mediated maintenance of cancer stem cell properties. Collectively, our findings provide direct evidence that AFP-driven stemness contributes functionally to HCC progression, establishing AFP as a molecular regulator rather than merely a diagnostic marker. This study elucidates a novel AFP-PI3K/Akt-stemness axis in HCC pathogenesis and highlights potential therapeutic targets for stemness-directed interventions in AFP-positive HCC.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"142 ","pages":"Article 112401"},"PeriodicalIF":3.7,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146122612","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}
引用次数: 0
1,2,3,6-Tetragalloylglucose inhibits hnRNPA2B1/TRAIL Axis to attenuate apoptosis and barrier dysfunction in intestinal epithelial cells: A potential therapeutic avenue for IBD. 1,2,3,6-四烯基葡萄糖抑制hnRNPA2B1/TRAIL轴减轻肠上皮细胞凋亡和屏障功能障碍:IBD的潜在治疗途径
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-04 DOI: 10.1016/j.cellsig.2026.112411
Chao Wang, Luyao Gao, Xiaoyu Lv, Junyan Wang, Yuanyuan Shen, Jiajia Wang, Qiao Mei, Futao Meng

Intestinal epithelial cells (IECs) injury and intestinal barrier function impairment are key risk factors for the pathogenesis and progression of inflammatory bowel disease (IBD). Heterogeneous nuclear ribonucleoprotein A2B1 (A2B1), as an N6-methyladenosine (m6A)-binding protein, is upregulated in intestinal epithelial cells of IBD patients. However, the role of m6A modifications and A2B1 in intestinal epithelial cell damage and intestinal barrier dysfunction remains largely unexplored. This study confirmed that A2B1 was significantly upregulated in IECs and tissues in IBD. Elevated expression of A2B1 was also found in tumor necrosis factor alpha (TNF-α) induced Caco-2 cells, intestinal organoids and dextran sulfate sodium (DSS) induced mouse model colon tissues. Overexpression of A2B1 in IECs led to increased apoptosis and barrier dysfunction, while knockdown of A2B1 ameliorated these effects. A2B1 interacted with TNF-related apoptosis inducing ligand (TRAIL) in an m6A dependent manner and regulated intestinal epithelial cell apoptosis and barrier function by modulating TRAIL expression. 1,2,3,6-Tetragalloylglucose (TeGG) was identified as a potent inhibitor of A2B1, effectively blocking TNF-α induced TRAIL upregulation and barrier damage in both cellular and organoid models. The study results suggest that A2B1 plays a crucial role in IBD by modulating TRAIL mRNA, leading to IECs apoptosis and intestinal barrier dysfunction. Targeting the A2B1-TRAIL interaction with small-molecule inhibitors like TeGG offers a novel and promising therapeutic approach for the treatment of IBD.

{"title":"1,2,3,6-Tetragalloylglucose inhibits hnRNPA2B1/TRAIL Axis to attenuate apoptosis and barrier dysfunction in intestinal epithelial cells: A potential therapeutic avenue for IBD.","authors":"Chao Wang, Luyao Gao, Xiaoyu Lv, Junyan Wang, Yuanyuan Shen, Jiajia Wang, Qiao Mei, Futao Meng","doi":"10.1016/j.cellsig.2026.112411","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112411","url":null,"abstract":"<p><p>Intestinal epithelial cells (IECs) injury and intestinal barrier function impairment are key risk factors for the pathogenesis and progression of inflammatory bowel disease (IBD). Heterogeneous nuclear ribonucleoprotein A2B1 (A2B1), as an N6-methyladenosine (m6A)-binding protein, is upregulated in intestinal epithelial cells of IBD patients. However, the role of m6A modifications and A2B1 in intestinal epithelial cell damage and intestinal barrier dysfunction remains largely unexplored. This study confirmed that A2B1 was significantly upregulated in IECs and tissues in IBD. Elevated expression of A2B1 was also found in tumor necrosis factor alpha (TNF-α) induced Caco-2 cells, intestinal organoids and dextran sulfate sodium (DSS) induced mouse model colon tissues. Overexpression of A2B1 in IECs led to increased apoptosis and barrier dysfunction, while knockdown of A2B1 ameliorated these effects. A2B1 interacted with TNF-related apoptosis inducing ligand (TRAIL) in an m6A dependent manner and regulated intestinal epithelial cell apoptosis and barrier function by modulating TRAIL expression. 1,2,3,6-Tetragalloylglucose (TeGG) was identified as a potent inhibitor of A2B1, effectively blocking TNF-α induced TRAIL upregulation and barrier damage in both cellular and organoid models. The study results suggest that A2B1 plays a crucial role in IBD by modulating TRAIL mRNA, leading to IECs apoptosis and intestinal barrier dysfunction. Targeting the A2B1-TRAIL interaction with small-molecule inhibitors like TeGG offers a novel and promising therapeutic approach for the treatment of IBD.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112411"},"PeriodicalIF":3.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131452","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}
引用次数: 0
ADAM12-programmed ECM-CAF remodeling activates PI3K-AKT and enforces an immune-excluded microenvironment to drive bladder cancer progression and therapy resistance. adam12编程的ECM-CAF重塑激活PI3K-AKT并强化免疫排斥微环境,从而推动膀胱癌的进展和治疗耐药性。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-04 DOI: 10.1016/j.cellsig.2026.112398
Tianbao Song, Wenlin He, Qin Yuan, Sihan Xia, Qin Yi, Yipeng He, Weimin Yu, Fan Cheng

Tumor-associated fibroblast-mediated matrix remodeling is an important feature of invasive immune-rejection bladder cancer, but its pathogenic mechanism and potential therapeutic targets are still unclear. The matrix and immune interaction network and core related genes in bladder cancer were systematically investigated by combining single-cell transcriptome data analysis and fibroblast GWAS data with TCGA and GEO data deconvolution, WGCNA, drug response prediction, multiplex immunofluorescence, and in vitro and in vivo validation experiments of cells and animals. ADAM12's functional validation. The findings demonstrated that the tumor-associated fibroblast ECM-CAF subgroup infiltration was evident in bladder cancer and was substantially associated with the upregulation of the core genes ADAM12 and TP53-biased basal-like program. These were characterized by the deposition of dense matrix, the upregulation of numerous immune checkpoints, the rejection and dysfunction of T cells, and a decrease in immunogenicity. Multiplex immunofluorescence localization of bladder cancer and normal bladder tissue showed that ADAM12 was significantly associated with the progression of non-muscle invasive bladder cancer to muscle invasive bladder cancer and the infiltration of ECM-CAF. Knockdown of ADAM12 inhibited the proliferation, migration, and invasion of bladder cancer cells, reduced the activation of the PI3K-AKT-mTOR pathway, and inhibited bladder cancer xenograft growth and lung metastasis. ADAM12 overexpression triggered the PI3K-AKT-mTOR pathway, enhanced the development and lung metastasis of bladder cancer xenografts, and markedly increased the invasion, migration, and proliferation of bladder cancer cells. The above results indicate that ADAM12, as a matrix-driven factor, links matrix remodeling, PI3K-AKT signaling pathway and bladder cancer immunosuppression, and has good prognostic and therapeutic stratification potential, providing new ideas for precision targeted intervention and treatment of bladder cancer.

{"title":"ADAM12-programmed ECM-CAF remodeling activates PI3K-AKT and enforces an immune-excluded microenvironment to drive bladder cancer progression and therapy resistance.","authors":"Tianbao Song, Wenlin He, Qin Yuan, Sihan Xia, Qin Yi, Yipeng He, Weimin Yu, Fan Cheng","doi":"10.1016/j.cellsig.2026.112398","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112398","url":null,"abstract":"<p><p>Tumor-associated fibroblast-mediated matrix remodeling is an important feature of invasive immune-rejection bladder cancer, but its pathogenic mechanism and potential therapeutic targets are still unclear. The matrix and immune interaction network and core related genes in bladder cancer were systematically investigated by combining single-cell transcriptome data analysis and fibroblast GWAS data with TCGA and GEO data deconvolution, WGCNA, drug response prediction, multiplex immunofluorescence, and in vitro and in vivo validation experiments of cells and animals. ADAM12's functional validation. The findings demonstrated that the tumor-associated fibroblast ECM-CAF subgroup infiltration was evident in bladder cancer and was substantially associated with the upregulation of the core genes ADAM12 and TP53-biased basal-like program. These were characterized by the deposition of dense matrix, the upregulation of numerous immune checkpoints, the rejection and dysfunction of T cells, and a decrease in immunogenicity. Multiplex immunofluorescence localization of bladder cancer and normal bladder tissue showed that ADAM12 was significantly associated with the progression of non-muscle invasive bladder cancer to muscle invasive bladder cancer and the infiltration of ECM-CAF. Knockdown of ADAM12 inhibited the proliferation, migration, and invasion of bladder cancer cells, reduced the activation of the PI3K-AKT-mTOR pathway, and inhibited bladder cancer xenograft growth and lung metastasis. ADAM12 overexpression triggered the PI3K-AKT-mTOR pathway, enhanced the development and lung metastasis of bladder cancer xenografts, and markedly increased the invasion, migration, and proliferation of bladder cancer cells. The above results indicate that ADAM12, as a matrix-driven factor, links matrix remodeling, PI3K-AKT signaling pathway and bladder cancer immunosuppression, and has good prognostic and therapeutic stratification potential, providing new ideas for precision targeted intervention and treatment of bladder cancer.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112398"},"PeriodicalIF":3.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131447","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}
引用次数: 0
Exploring the role and potential mechanisms of SIK1 in cartilage damage in osteoarthritis based on metabolomics. 基于代谢组学探讨SIK1在骨关节炎软骨损伤中的作用及潜在机制。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-04 DOI: 10.1016/j.cellsig.2026.112407
Gang Kong, Li Chen, Qi Zhang, Jingbo Pan, Kegui Liu

Objective: To investigate the role of salt induced kinases 1 (SIK1) in osteoarthritis (OA)-related cartilage damage and its underlying metabolic mechanisms.

Methods: An OA mouse model was established using destabilization of the medial meniscus (DMM) technique. Pathological changes in cartilage tissue were evaluated using hematoxylin-eosin staining (HE) and safranin O-fast green staining. SIK1 expression levels in OA mice were assessed using immunohistochemistry and Western blot analysis. Metabolomic analysis revealed differential metabolites and signaling pathways between normal and OA mice. An adeno-associated virus (AAV) overexpressing SIK1 was constructed and used to transfect interleukin-1β (IL-1β) induced chondrocytes. Chondrocyte survival rate, DNA damage, inflammatory response, matrix degradation, and metabolic markers were assessed using CCK8 assays, immunofluorescence, ELISA, and Western blot. Subsequently, arachidonic acid (AA) was introduced to activate specific metabolic pathways, and in vivo changes in cartilage damage and metabolic homeostasis were evaluated.

Results: SIK1 expression was significantly downregulated in the cartilage of OA mice. Compared with the Model group, SIK1 overexpression significantly improved cartilage degeneration, reduced extracellular matrix (ECM) degradation, and lowered the Mankin score. Metabolomic analysis revealed significant activation of the AA metabolic pathway in the OA model group. SIK1 overexpression protected chondrocytes from IL-1β-induced apoptosis and inflammation. It also maintained ECM balance by increasing collagen II and aggrecan while decreasing matrix metallopeptidase 13 (MMP13). Mechanistically, AA intervention reversed the protective effects of SIK1 overexpression against OA chondrocyte injury.

Conclusion: SIK1 ameliorated OA-related cartilage damage by inhibiting AA metabolic pathway.

{"title":"Exploring the role and potential mechanisms of SIK1 in cartilage damage in osteoarthritis based on metabolomics.","authors":"Gang Kong, Li Chen, Qi Zhang, Jingbo Pan, Kegui Liu","doi":"10.1016/j.cellsig.2026.112407","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112407","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of salt induced kinases 1 (SIK1) in osteoarthritis (OA)-related cartilage damage and its underlying metabolic mechanisms.</p><p><strong>Methods: </strong>An OA mouse model was established using destabilization of the medial meniscus (DMM) technique. Pathological changes in cartilage tissue were evaluated using hematoxylin-eosin staining (HE) and safranin O-fast green staining. SIK1 expression levels in OA mice were assessed using immunohistochemistry and Western blot analysis. Metabolomic analysis revealed differential metabolites and signaling pathways between normal and OA mice. An adeno-associated virus (AAV) overexpressing SIK1 was constructed and used to transfect interleukin-1β (IL-1β) induced chondrocytes. Chondrocyte survival rate, DNA damage, inflammatory response, matrix degradation, and metabolic markers were assessed using CCK8 assays, immunofluorescence, ELISA, and Western blot. Subsequently, arachidonic acid (AA) was introduced to activate specific metabolic pathways, and in vivo changes in cartilage damage and metabolic homeostasis were evaluated.</p><p><strong>Results: </strong>SIK1 expression was significantly downregulated in the cartilage of OA mice. Compared with the Model group, SIK1 overexpression significantly improved cartilage degeneration, reduced extracellular matrix (ECM) degradation, and lowered the Mankin score. Metabolomic analysis revealed significant activation of the AA metabolic pathway in the OA model group. SIK1 overexpression protected chondrocytes from IL-1β-induced apoptosis and inflammation. It also maintained ECM balance by increasing collagen II and aggrecan while decreasing matrix metallopeptidase 13 (MMP13). Mechanistically, AA intervention reversed the protective effects of SIK1 overexpression against OA chondrocyte injury.</p><p><strong>Conclusion: </strong>SIK1 ameliorated OA-related cartilage damage by inhibiting AA metabolic pathway.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112407"},"PeriodicalIF":3.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131470","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}
引用次数: 0
Multi-omics reveals that CTHRC1 secreted by cancer-associated fibroblasts promotes EMT by ITGA5/PI3K/AKT signaling pathway in HNSCC. 多组学研究表明,癌症相关成纤维细胞分泌的CTHRC1通过ITGA5/PI3K/AKT信号通路促进HNSCC的EMT。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-04 DOI: 10.1016/j.cellsig.2026.112409
Yang Wu, Tian Chen, Jingjing Zuo, Tao Shen, Lin Dong, Fen Li, Lei Wang, Zezhang Tao

Background: Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy with poor prognosis. Cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME) drive tumor progression through complex cellular interactions; however, the key functional molecules and underlying mechanisms of CAFs in HNSCC remain unclear.

Methods: We employed single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) to characterize the heterogeneity of the HNSCC TME. Survival analysis, immune infiltration assessment and immune treatment response evaluation were evaluated based on TCGA and multiple GEO cohorts. Key findings were further validated through a series of functional experiments in vitro and in vivo.

Results: Multimodal omics analysis revealed that CTHRC1 expression was specifically enriched in the CAFs subpopulation. These CTHRC1+ CAFs were spatially co-localized with regions exhibiting epithelial-mesenchymal transition (EMT) and angiogenesis signatures in HNSCC. High infiltration of CTHRC1+ CAFs was significantly associated with poor patient prognosis. The tumor immune dysfunction and exclusion (TIDE) analysis indicated that high expression of CTHRC1 was associated with immunosuppression and adverse reactions to immunotherapy. Functional studies demonstrated that CAFs-secreted CTHRC1 directly binds to ITGA5 on tumor cells, activating the PI3K/AKT signaling pathway, thereby promoting proliferation, EMT, and angiogenesis in HNSCC.

Conclusions: This study has confirmed that CTHRC1+ CAFs facilitate HNSCC malignancy via the ITGA5/PI3K/AKT signaling axis. These findings highlight CTHRC1 as a potential prognostic biomarker and therapeutic target in HNSCC.

{"title":"Multi-omics reveals that CTHRC1 secreted by cancer-associated fibroblasts promotes EMT by ITGA5/PI3K/AKT signaling pathway in HNSCC.","authors":"Yang Wu, Tian Chen, Jingjing Zuo, Tao Shen, Lin Dong, Fen Li, Lei Wang, Zezhang Tao","doi":"10.1016/j.cellsig.2026.112409","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112409","url":null,"abstract":"<p><strong>Background: </strong>Head and neck squamous cell carcinoma (HNSCC) is a highly aggressive malignancy with poor prognosis. Cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME) drive tumor progression through complex cellular interactions; however, the key functional molecules and underlying mechanisms of CAFs in HNSCC remain unclear.</p><p><strong>Methods: </strong>We employed single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) to characterize the heterogeneity of the HNSCC TME. Survival analysis, immune infiltration assessment and immune treatment response evaluation were evaluated based on TCGA and multiple GEO cohorts. Key findings were further validated through a series of functional experiments in vitro and in vivo.</p><p><strong>Results: </strong>Multimodal omics analysis revealed that CTHRC1 expression was specifically enriched in the CAFs subpopulation. These CTHRC1<sup>+</sup> CAFs were spatially co-localized with regions exhibiting epithelial-mesenchymal transition (EMT) and angiogenesis signatures in HNSCC. High infiltration of CTHRC1<sup>+</sup> CAFs was significantly associated with poor patient prognosis. The tumor immune dysfunction and exclusion (TIDE) analysis indicated that high expression of CTHRC1 was associated with immunosuppression and adverse reactions to immunotherapy. Functional studies demonstrated that CAFs-secreted CTHRC1 directly binds to ITGA5 on tumor cells, activating the PI3K/AKT signaling pathway, thereby promoting proliferation, EMT, and angiogenesis in HNSCC.</p><p><strong>Conclusions: </strong>This study has confirmed that CTHRC1<sup>+</sup> CAFs facilitate HNSCC malignancy via the ITGA5/PI3K/AKT signaling axis. These findings highlight CTHRC1 as a potential prognostic biomarker and therapeutic target in HNSCC.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112409"},"PeriodicalIF":3.7,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131458","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}
引用次数: 0
KLF2 interacts with AP-1 to negatively affect osteoclast differentiation and activity. KLF2与AP-1相互作用,对破骨细胞的分化和活性产生负面影响。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-03 DOI: 10.1016/j.cellsig.2026.112406
Sijun Liu, Shasha Tu, Mengmeng Duan, Jiazhou Li, Li Zhang, Jie Ren, Ting Zhao, Jing Xie, Xiaoheng Liu

Osteoclasts function as the primary effectors of bone resorption and are essential for bone homeostasis. Krüppel-like factor 2 (KLF2) has been implicated in osteoclast differentiation, but its precise mechanism remains poorly understood. In this study, we aimed to investigate the role of KLF2 in osteoclast function by characterising osteoclastogenesis, maturation and activity and to explore the underlying biomechanism. We showed that KLF2 negatively regulates osteoclastogenesis by characterising the osteoclast number, size and protein markers; that it negatively regulates osteoclast maturation by characterising the formation of intact actin rings and punctured podosome clusters; and that it negatively regulates osteoclast activity by characterising intracellular acidification through KLF2 overexpression by lentiviral transfection and KLF2 knockdown by small interfering RNA (siRNA) transfection. The results of chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (Co-IP) assays revealed that KLF2 directly interacted with c-Fos and c-Jun, which together constitute the activator protein-1 (AP-1) complex. By overexpressing KLF2 and knockdown with si-KLF2, we revealed that KLF2 mediated osteoclast function via negative regulation of the AP-1 complex. The inhibition of AP-1 activity confirmed its importance in KLF2-mediated osteoclast differentiation; Moreover, the inhibition of JNK signalling decreased the AP-1 activation induced by KLF2 knockdown, indicating the importance of the RANKL-MAPK-AP-1-NFATc1 axis in KLF2-regulated osteoclast differentiation. This study reveals a typical type of negative regulation of osteoclasts by KLF2 and provides information for potential therapeutic targets in osteolytic diseases, including osteoporosis.

{"title":"KLF2 interacts with AP-1 to negatively affect osteoclast differentiation and activity.","authors":"Sijun Liu, Shasha Tu, Mengmeng Duan, Jiazhou Li, Li Zhang, Jie Ren, Ting Zhao, Jing Xie, Xiaoheng Liu","doi":"10.1016/j.cellsig.2026.112406","DOIUrl":"https://doi.org/10.1016/j.cellsig.2026.112406","url":null,"abstract":"<p><p>Osteoclasts function as the primary effectors of bone resorption and are essential for bone homeostasis. Krüppel-like factor 2 (KLF2) has been implicated in osteoclast differentiation, but its precise mechanism remains poorly understood. In this study, we aimed to investigate the role of KLF2 in osteoclast function by characterising osteoclastogenesis, maturation and activity and to explore the underlying biomechanism. We showed that KLF2 negatively regulates osteoclastogenesis by characterising the osteoclast number, size and protein markers; that it negatively regulates osteoclast maturation by characterising the formation of intact actin rings and punctured podosome clusters; and that it negatively regulates osteoclast activity by characterising intracellular acidification through KLF2 overexpression by lentiviral transfection and KLF2 knockdown by small interfering RNA (siRNA) transfection. The results of chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (Co-IP) assays revealed that KLF2 directly interacted with c-Fos and c-Jun, which together constitute the activator protein-1 (AP-1) complex. By overexpressing KLF2 and knockdown with si-KLF2, we revealed that KLF2 mediated osteoclast function via negative regulation of the AP-1 complex. The inhibition of AP-1 activity confirmed its importance in KLF2-mediated osteoclast differentiation; Moreover, the inhibition of JNK signalling decreased the AP-1 activation induced by KLF2 knockdown, indicating the importance of the RANKL-MAPK-AP-1-NFATc1 axis in KLF2-regulated osteoclast differentiation. This study reveals a typical type of negative regulation of osteoclasts by KLF2 and provides information for potential therapeutic targets in osteolytic diseases, including osteoporosis.</p>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":" ","pages":"112406"},"PeriodicalIF":3.7,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123887","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}
引用次数: 0
Extracellular vesicles derived from HSCs transmitted circPVT1 to ameliorate oxidative damage to hepatocytes by targeting the miR-125b-5p/BCL2L2 signalling pathway. 来源于造血干细胞的细胞外囊泡通过靶向miR-125b-5p/BCL2L2信号通路,传递circPVT1以改善肝细胞的氧化损伤。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-02-01 DOI: 10.1016/j.cellsig.2026.112405
Yan Wang, Anzhi Chang, Qunyu Huang, Zhirong Ye, Yunfa Ding, Chengbin Li, Quan Feng, Yuanlin Zou, Shigang Duan, Fanbing Wang, Huilai Miao

Our previous studies demonstrated that extracellular vesicles (EVs) derived from quiescent hepatic stellate cells (HSC-EVs) exert protective effects against oxidative injury to hepatocytes. In this study, we aimed to clarify the hepatoprotective mechanisms of action of HSC-EVs. By RNA sequencing, circPVT1 was identified as a highly abundant circular RNA in HSC-EVs. Functionally, we observed that circPVT1 knockdown abolished the beneficial effects of HSC-EVs in improving liver function and increasing the proliferation and reducing the apoptosis of hepatocytes in a H₂O₂-treated hepatocyte model and in a CCL₄-induced liver injury rat model via delivering circPVT1. Bioinformatics analysis and dual luciferase assays revealed that circPVT1 acts as a molecular sponge for miR-125b-5p. Through a series of loss-and-gain experiments, we confirmed that circPVT1 increased the proliferation and reduced the apoptosis of hepatocytes through the inhibition of miR-125b-5p expression. Furthermore, rescue experiments revealed that silencing BCL2L2, a target gene of miR-125b-5p, prevented the enhancement of hepatoprotection by HSC-EVs combined with miR-125b-5p inhibition. These findings demonstrate that HSC-EVs are potential therapeutic vesicles that can protect against oxidative injury to hepatocytes through the activation of the circPVT1/miR-125b-5p/BCL2L2 signalling pathway.

我们之前的研究表明,来自静止肝星状细胞(hsc - ev)的细胞外囊泡(ev)对肝细胞的氧化损伤具有保护作用。在本研究中,我们旨在阐明hsc - ev的肝保护作用机制。通过RNA测序,circPVT1在hsc - ev中被鉴定为高丰度的环状RNA。在功能上,我们观察到通过传递circPVT1,在h2o2处理的肝细胞模型和CCL 4诱导的肝损伤大鼠模型中,circPVT1敲低可消除hsc - ev改善肝功能、增加肝细胞增殖和减少肝细胞凋亡的有益作用。生物信息学分析和双荧光素酶测定显示circPVT1作为miR-125b-5p的分子海绵。通过一系列的失得实验,我们证实circPVT1通过抑制miR-125b-5p的表达,增加肝细胞的增殖,减少肝细胞的凋亡。此外,救援实验显示,沉默miR-125b-5p的靶基因BCL2L2,阻止了hsc - ev联合miR-125b-5p抑制对肝保护的增强。这些发现表明,hsc - ev是潜在的治疗性囊泡,可以通过激活circPVT1/miR-125b-5p/BCL2L2信号通路来保护肝细胞免受氧化损伤。
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引用次数: 0
Potential role of splice junctions of α-synuclein isoforms in the activation of T-cells: Implications for Parkinson's disease. α-突触核蛋白亚型剪接在t细胞活化中的潜在作用:对帕金森病的影响
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-01-31 DOI: 10.1016/j.cellsig.2026.112399
Shweta Kaul, Aravind Vulli, Shasi V Kalivendi

α-Synuclein (α-syn) aggregate-mediated loss of dopaminergic neurons play a critical role in the mechanisms mediating Parkinson's disease (PD). While neuroinflammation is invariably associated with several neurodegenerative disorders, emerging reports on the N- and C-terminus epitopes of α-syn in inducing activated T-cells/microglia garnered much attention. Interestingly, differential expression of isoforms of α-syn with altered N- and C-terminus regions were also noticed in PD subjects; however, their role in the activation of T-cells is not yet known. Hence, we sought to investigate the effect of monomeric and aggregated α-syn-spliced isoforms on activation of T-cells. Our results indicate that, as compared to monomeric forms, stereotaxic administration of PFFs of Wild Type (WT-syn) and 112-syn-induced significant loss of SNPc dopamine neurons and motor coordination. Further, the expression of CD4+ and CD8+ T-cells was significantly elevated by PFFs of WT and 112-syn as compared to their corresponding monomers. Peripheral blood mononuclear cells (PBMCs) isolated from mice administered with PFFs exhibited increased cytokine responses upon stimulation with peptides corresponding to the C-terminus region of WT-syn and 112-syn, suggesting their antigenic potential in the order WT-syn < 112-syn. This enhanced antigenicity of 112-syn indicate that the spliced α-syn isoforms, particularly 112-syn, could play a critical role in immune activation in PD, highlighting splice junctions as potential targets for therapeutic strategies.

α-突触核蛋白(α-syn)聚集物介导的多巴胺能神经元损失在帕金森病(PD)的机制中起关键作用。虽然神经炎症总是与几种神经退行性疾病相关,但α-syn的N端和c端表位在诱导活化t细胞/小胶质细胞方面的新报道引起了人们的广泛关注。有趣的是,PD受试者中α-syn同工型的差异表达与N端和c端区域的改变也被注意到;然而,它们在t细胞活化中的作用尚不清楚。因此,我们试图研究单体和聚集的α-syn剪接异构体对t细胞活化的影响。我们的研究结果表明,与单体形式相比,野生型(WT-syn)和112-syn的立体定向给药会导致SNPc多巴胺神经元和运动协调性的显著丧失。此外,与相应的单体相比,WT和112-syn的pff显著提高了CD4+和CD8+ t细胞的表达。经pff处理的小鼠外周血单核细胞(pmcs)在WT-syn和112-syn的c端对应肽的刺激下表现出增强的细胞因子反应,表明它们具有WT-syn序列的抗原性
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引用次数: 0
Riluzole preserves brain endothelial integrity in ischemic stroke via SLC7A11-dependent GPX4 and HIF-1α/VEGFA signaling 利鲁唑通过slc7a11依赖性GPX4和HIF-1α/VEGFA信号通路保护缺血性脑卒中的脑内皮完整性。
IF 3.7 2区 生物学 Q2 CELL BIOLOGY Pub Date : 2026-01-31 DOI: 10.1016/j.cellsig.2026.112378
Haipeng Wang , Ying Feng , Wei Jiang , Han Wang , Ruolin Zhang , Guangqiang Li , Chao Duan , Yuneng Zhou , Wendai Bao , Ke Shui , Min Zhang , Zhibing Ai , Xin Yang , Peiyang Zhou , Zhiqiang Dong
Riluzole, an FDA-approved neuroprotective agent, was investigated for its therapeutic potential in ischemic stroke. Transcriptomic profiling of human brain microvascular endothelial cells (hBMECs) subjected to oxygen-glucose deprivation/reperfusion (OGD/R) identified a pivotal role for the cystine/glutamate antiporter SLC7A11. We found that riluzole activates SLC7A11, thereby triggering a dual protective mechanism: it strengthens cellular antioxidant capacity by upregulating GPX4 while simultaneously enhancing proangiogenic signaling through the HIF-1α/VEGFA pathway. Consequently, riluzole attenuated OGD/R-induced endothelial injury and, in a mouse stroke model, reduced blood–brain barrier disruption and improved neurological outcomes. Our study reveals a previously unrecognized cerebrovascular protective mechanism of riluzole, establishing SLC7A11 as its key mediator. This SLC7A11-dependent dual-pathway action represents a substantive advance in understanding riluzole's therapeutic biology beyond its established roles in the central nervous system.
利鲁唑是一种经fda批准的神经保护剂,研究其治疗缺血性中风的潜力。缺氧-葡萄糖剥夺/再灌注(OGD/R)的人脑微血管内皮细胞(hBMECs)的转录组学分析发现了胱氨酸/谷氨酸反转运蛋白SLC7A11的关键作用。我们发现利鲁唑激活SLC7A11,从而触发双重保护机制:它通过上调GPX4来增强细胞抗氧化能力,同时通过HIF-1α/VEGFA途径增强促血管生成信号。因此,利鲁唑减轻了OGD/ r诱导的内皮损伤,在小鼠中风模型中,减少了血脑屏障的破坏,改善了神经系统的预后。本研究揭示了利鲁唑的脑血管保护机制,确定了SLC7A11为其关键介质。这种slc7a11依赖的双途径作用代表了对利鲁唑治疗生物学的实质性进展,超越了其在中枢神经系统中的既定作用。
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引用次数: 0
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Cellular signalling
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