Ask about this productRelated genes to: Itgb1 antibody
- Gene:
- ITGB1 NIH gene
- Name:
- integrin subunit beta 1
- Previous symbol:
- FNRB, MSK12, MDF2
- Synonyms:
- CD29, GPIIA
- Chromosome:
- 10p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-27
- Date modifiied:
- 2016-10-05
Related products to: Itgb1 antibody
Related articles to: Itgb1 antibody
- Type X collagen (COL10A1) is an extracellular matrix protein primarily expressed by hypertrophic chondrocytes and is essential for endochondral ossification and skeletal mineralization. Although traditionally regarded as cartilage-specific, recent studies have reported its re-expression in a range of solid tumors. This shift in expression pattern suggests that COL10A1 may have functions beyond development, particularly within the tumor microenvironment (TME). Elevated COL10A1 levels have been reported in cancers such as breast, gastric, colorectal, and lung cancers, where both tissue expression and circulating levels are frequently associated with advanced disease stage and poor clinical outcomes. These observations support COL10A1 as a potential diagnostic and prognostic biomarker. Beyond its clinical associations, accumulating evidence indicates that COL10A1 actively contributes to tumor progression. It is involved in extracellular matrix remodeling, angiogenesis, epithelial-mesenchymal transition (EMT), and alterations in immune cell infiltration, and possibly immunotherapy response. In addition, its enrichment in specific subsets of cancer-associated fibroblasts (CAFs) highlights its essential role in tumor-stroma interactions. At the mechanistic level, COL10A1 has been linked to multiple oncogenic signaling pathways, including TGF-β1/SOX9, as well as downstream DDR2/FAK and ITGB1/PI3K/AKT pathways, which may collectively promote tumor invasion, metastasis, and therapy resistance. However, its biological functions are not yet fully defined, and tumor heterogeneity continues to complicate its clinical application. Further studies are needed to clarify how COL10A1-functions within the tumor microenvironment and to determine its clinical value as a biomarker and a potential therapeutic target in solid cancers. - Source: PubMed
Publication date: 2026/04/15
Zhu TianxiangLiang YutingDong WanyuDeng RushuangHu WenshiWei RongWang QianLu YaojuanQiao LongweiHe Tong-ChuanZheng Qiping - Aberrant protein glycosylation contributes significantly to hepatocellular carcinoma (HCC) progression. β-1,4-Galactosyltransferase 3 (B4GALT3), an enzyme involved in glycosylation, is overexpressed in HCC and promotes tumour growth by stabilizing integrin β1 (ITGB1). This study aimed to evaluate B4GALT3 as a therapeutic target and develop a precision nanotherapeutic approach for HCC. - Source: PubMed
Publication date: 2026/05/19
Yu XiaohuiChen XiaoyanGuo HuiJin XiaTan PingpingZeng LongwuHe YanLi Junjun - Pancreatic ductal adenocarcinoma (PDAC) is characterized by a highly immunosuppressive and desmoplastic tumor microenvironment (TME) that limits the efficacy of immunotherapy. However, the evolution of this immunosuppressive TME and the underlying mechanisms remain incompletely understood. Here, we construct a dynamic single-cell atlas spanning uninvolved adjacent pancreatic tissue (UNIN), intraductal papillary mucinous neoplasm (IPMN), and PDAC. We confirm the stepwise establishment of an immunosuppressive milieu, accompanied by the emergence of LRRC15 fibroblasts as determinants. Functional assays further identify tumor-derived LAMB3 as a regulator of LRRC15 fibroblast differentiation. Mechanistically, LAMB3 promotes FOSL2-dependent transcriptional activation of LRRC15 through the ITGB1/FAK/MAPK signaling axis, ultimately suppressing T cell cytotoxicity. Orthotopic models reveal that LAMB3 overexpression increases the LRRC15 positive area and impairs T cell cytotoxicity, whereas FAK inhibition partially reverses these effects. In parallel, LAMB3 knockdown reduces the LRRC15 positive area and improves the efficacy of PD-1 blockade. Moreover, glycolytic reprogramming in PDAC ductal cells upregulates LAMB3 expression and correlates with increased LRRC15 fibroblast enrichment. Clinically, co-enrichment of LAMB3 PDAC ductal cells and LRRC15 fibroblasts is associated with inferior overall survival. Collectively, our findings define a dynamic ductal-fibroblast-immune multicellular axis underlying PDAC pathogenesis and provide insights into potential therapeutic strategies. - Source: PubMed
Publication date: 2026/05/19
Shi XuqingLiu HangqiSun JianruLiu XiaodingJv XinpingChen LongyunZhang YuhanZhang HuiXing XudongLi RuiyuKe XinyiWang JunYin XianglinLiu BohanLiu QixianWang YuanLu JunliangLiu ShiyiPang JunyiCai YumengDai MenghuaBai FanWu HuanwenLiang Zhiyong - Metabolic reprogramming is a hallmark of hepatocellular carcinoma (HCC), and amino acid reprogramming plays an important role in its metastatic progression. However, the function of amino acid reprogramming in HCC metastatic progression remains unclear. This study aimed to elucidate the function and mechanism of amino acid reprogramming, particularly focusing on proline metabolism, in driving HCC metastasis. HCC cohort and multiple HCC models were enrolled to investigate the role of amino acid reprogramming in HCC metastatic progression. The pro-metastatic effect of l-proline in HCC was consistently validated across in vitro and in vivo studies. Ribosome profiling (Ribo-seq) and l-proline pull-down were used to investigate the mechanism of proline-mediated HCC metastasis. Based on metabolomics and proteomics, we found that proline metabolism was enhanced during HCC metastasis, as evidenced by increased proline levels and proline metabolism-related enzymes in both HCC metastatic patients and mice. Moreover, high levels of proline were found to promote HCC metastasis. Mechanistically, l-proline directly interacted with glutamyl-prolyl-tRNA synthetase 1 (EPRS1) at its Glu residue, thereby selectively enhancing the translation of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA), AKT serine/threonine kinase 3 (AKT3), and integrin subunit β1 (ITGB1). Importantly, the enhanced protein translation could be abolished by bersiporocin, an EPRS1 inhibitor that prevents l-proline binding to EPRS1. Finally, the inhibitory effect of bersiporocin on HCC metastasis was confirmed in patient-derived orthotopic xenograft models. Our findings not only revealed the critical role of l-proline-bound EPRS1 in promoting HCC metastasis but also indicated that inhibiting this binding could be a promising strategy to prevent metastasis. - Source: PubMed
Publication date: 2026/05/14
Zhang HuiGu LeirongSu XiamengChen WanjinTan MingYu HaiboZhou HongzhongGao TingtingWang ZhilingChen XinyanChen WeixianChen JuanCheng Shengtao - Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with poor prognosis, characterized by a desmoplastic tumor microenvironment (TME) that limits immune cell infiltration and diminishes response to immunotherapy. Arylacetamide deacetylase (AADAC) is a lipid-processing enzyme, but its role in tumor progression, stromal organization, and immune modulation remains unclear. - Source: PubMed
Publication date: 2026/05/08
Wu ChaoYang Jun