Fig. 4

ITGB1 and cell proliferation and apoptosis. In cancer cells, ITGB1 is involved in controlling cell proliferation or apoptosis pathways. The downregulation of ITGB1 in liver cells leads to dephosphorylation of c-Met and EGFR, thereby inhibiting cell proliferation. The ITGB1/PXN/YWHAZ/AKT axis promotes the development of HCC by accelerating the cell cycle process. In addition, knocking down CSN5 can lower ITGB1 and CDK6, activating the NF-κB and other signaling pathways that lead to cell apoptosis. CYR61/CCN1 can be achieved by combining α1/β1 integrin, inhibition of the ITGB1 expression, and stimulation of intracellular ROS accumulation can suppress the activation of the EGFR signaling pathway and the proliferation of HCC cells. In GC, BCL9L is activated by ITGB1, β-catenin signaling pathway can enhance cell cloning and proliferation, and then the anti-apoptotic protein BCL2 is also activated. In CRC, overexpression of ITGB1 increases the BCL2 level while reducing the expression levels of autophagy related proteins such as Bax, caspase-3, and caspase-9. In addition, it increases CCND1 while reducing the level of p21. In PDAC, FxOH reduces apoptosis of PANC-1 cells by upregulating the expression of ITGB1, FAK, PXN, FYN, AKT, and PPAR. In BC, increased expression of α6/β1 integrin can decrease the number of non-receptor tyrosine kinase FERs in the cytoplasm, thereby weakening the ability of cells to resist apoptosis. Melanoma cells produce TIMP1, which helps them overcome apoptosis by constructing complexes with CD63 and ITGB1. In OC, ZNF304 can enhance cellular resistance to apoptosis by controlling ITGB1 transcription