Knockdown of Integrin α3 (ITGA3)-mediated proliferation and invasive activity by regulating the expression of N-cadherin and cyclin D1 in glioblastoma cells

The cell membrane protein Integrin α3 (ITGA3) acts as a crucial cell surface adhesion molecule and has emerged as a potential molecular marker across various cancers. Our study aimed to explore the biological role of ITGA3 in human Glioblastoma (GBM), an area yet to be thoroughly investigated. Initially, we assessed ITGA3 expression in glioma TMA tissue samples through immunohistochemistry analysis. Subsequently, we employed short interfering RNA (siRNA) to silence ITGA3 expression in different GBM cell lines and examined its impact on proliferation, invasion, adhesion, and migration assays. Furthermore, we conducted western blot analyses to gauge the expression levels of ITGA3, N-cadherin, and Cyclin D1 signaling molecules in glioma cells. Our findings revealed a significant correlation between elevated ITGA3 expression and poorer survival rates in patients with astrocytoma and glioma compared to those with low ITGA3 expression. Notably, silencing ITGA3 curbed cell proliferation and hindered cell mobility in glioma, potentially by impeding N-cadherin and Cyclin D1 signaling pathways. Collectively, our results pinpoint ITGA3 as an oncogenic biomarker, with its knockdown showcasing a potential to restrain the metastatic capabilities of GBM cells.