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Gene expression profiles associated with ITGBL1 overexpression

ABSTRACT: Gene expression profiles associated with ITGBL1 overexpression

PROVIDER: PRJNA699005 | ENA |

REPOSITORIES: ENA

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Gene expression profiles associated with ITGBL1 overexpression

Project description:In our previous microarray study we identified two subgroups of high-grade serous ovarian cancers with distinct gene expression and different survival. Among differentially expressed genes was an Integrin beta-like 1 (ITGBL1), coding for a poorly characterized protein comprised of ten EGF-like repeats. In this study we investigated ITGBL1 influence on ovarian cancer cells phenotype. Using various functional assays we found that ITGBL1 overexpression affected cellular adhesion, migration and invasiveness, while it had no effect on proliferation rate and the cell cycle. ITGBL1-overexpressing cells were significantly more resistant to cisplatin and paclitaxel, major drugs used in ovarian cancer treatment. Global gene expression analysis revealed that signaling pathways affected by ITGBL1 overexpression were mostly those related to extracellular matrix organization and function, integrin signaling, focal adhesion, cellular communication and motility; these results were consistent with the findings of our functional studies. Overall, our results indicate that higher expression of ITGBL1 in ovarian cancer is associated with features that may worsen clinical course of the disease.

2021-02-03 | GSE166029 | GEO

Bulk transcriptomic profiling reveal the epithelial-protective role of ITGBL1 during the progression of colitis

Project description:Inflammatory bowel disease (IBD) is characterized by progressive epithelial injury, chronic inflammation, and impaired intestinal barrier function. To comprehensively delineate the epithelial alterations and stress-related responses that occur during colitis progression, we investigated the functional role of integrin beta-like 1 (ITGBL1) in intestinal epithelial cells (IECs). Using patient specimens and DSS-induced colitis models, we identified marked upregulation of ITGBL1 in inflamed intestinal tissues. Loss of ITGBL1 resulted in the emergence of ferroptosis-prone epithelial subsets exhibiting elevated ACSL4 expression, lipid peroxidation, mitochondrial shrinkage, and enhanced oxidative stress, all of which were associated with aggravated epithelial damage and worse inflammatory outcomes. We further demonstrated that ITGBL1 deficiency activated the ANGPT2/PI3K-AKT signaling axis in IECs, leading to exaggerated oxidative stress and ferroptosis, accompanied by reduced expression of key tight-junction proteins including E-cadherin, ZO-1, occludin, and claudin-1. These alterations impaired epithelial cohesion and barrier integrity during disease progression. In contrast, supplementation with recombinant ITGBL1 suppressed ANGPT2 expression, mitigated PI3K-AKT hyperactivation, restored mitochondrial structure, alleviated ferroptosis, and improved epithelial barrier function. In conclusion, ITGBL1 serves as a critical regulator of epithelial stress responses and barrier stability during colitis, acting by restraining ANGPT2-mediated PI3K-AKT activation and ferroptotic cell death. These findings highlight a previously unrecognized epithelial-protective mechanism and identify the ITGBL1–ANGPT2 axis as a potential therapeutic target in IBD.

2025-12-31 | GSE314630 | GEO

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