Correlation of integrin alpha 7 with clinicopathological characteristics and survival profiles, as well as its regulatory role in cell proliferation, apoptosis, and stemness in non-small-cell lung cancer.

Abstract

BackgroundThe present study aimed to evaluate the correlation of integrin alpha 7 (ITGA7) with patients' clinicopathological characteristics and survival profiles, as well as its influence on cell proliferation, apoptosis, and stemness in non–small‐cell lung cancer (NSCLC).MethodsA total of 397 NSCLC patients underwent surgical resection were included, and ITGA7 was measured in tumor tissues and adjacent tissues by immunohistochemistry. patients' clinical data were extracted from database, and follow‐up records were reviewed. In cellular experiments, expression of ITGA7 was measured in NSCLC cell lines and normal human lung epithelial cell line by RT‐qPCR. The influence of ITGA7 on cell activity was assessed by transfecting overexpression plasmids and knockdown plasmids of ITGA7 into A549 cells.ResultsIntegrin alpha 7 was upregulated in tumor tissues compared with the adjacent tissues of NSCLC patients. Patients with ITGA7 high expression presented poorer pathological differentiation, larger tumor size, and more advanced TNM stage compared with patients with ITGA7 low expression. For survival profiles, both disease‐free survival and overall survival were shorter in ITGA7 high expression patients compared with ITGA7 low expression patients. In cellular experiments, ITGA7 was upregulated in NCI‐H1650, A549, HCC‐827, and NCI‐H1299 cells compared with normal human lung epithelial cells BEAS‐2B. In addition, ITGA7 promoted cell proliferation, inhibited cell apoptosis, and facilitated cell stemness in A549 cells.ConclusionIntegrin alpha 7 correlates with poor clinicopathological characteristics and survival profiles, and it promotes cell proliferation, stemness but suppresses cell apoptosis in NSCLC.