TRIM27 is Involved in the Viability and Metastasis of Lung Squamous Cell Carcinoma Cells via the PI3K/AKT Axis

Abstract

Background: Lung squamous cell carcinoma (LUSC) is one of the familiar types of lung cancer, but the molecular mechanism of LUSC progression remains unclear. The aim of this study is to investigate the biological function of tripartite motif-containing protein 27 (TRIM27) on LUSC progression. Methods: Cell immunochemistry, quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and cell transfection were used to detect the expression efficiencies of TRIM27, phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT), and phosphorylated AKT (pAKT) and the regulatory mechanism of these molecules. Cell Counting Kit-8 (CCK-8) assay, Transwell assay, and flow cytometry were used to detect the viability, metastasis, and apoptosis of LUSC cells. Results: Our data indicate that TRIM27 is overexpressed in LUSC. Up-regulation of TRIM27 increases the viability and metastasis of LUSC cells and suppresses apoptosis. The PI3K/AKT pathway is highly active in LUSC. TRIM27 knockdown reduces the expression efficiencies of PI3K, AKT, and pAKT. The addition of v-PI3K plasmid or v-AKT plasmid reverses the silencing of the TRIM27-induced inhibitory effect on LUSC cells. Conclusion: Our research demonstrates that TRIM27 promotes LUSC cell viability and metastasis by affecting the PI3K/AKT axis. We conclude that the TRIM27-PI3K/AKT axis plays a crucial role in LUSC.