Effect of SIRT6 Silencing On Post-Translational Modification of AKT Signalling Pathway in Non-Small Cell Lung Cancer Cell Lines

Abstract

SIRT6 has been suggested that SIRT6 functions in cells as a helpful modulator and tumor suppressor. Because the induction or blocking of apoptosis affects the course of cancer, SIRT6 has a dual function in the growth and spread of tumors. This study aims to investigate the post transilational modification at AKT signaling pathway under SIRT6 slicening. The main objectives are Silencing SIRT6 by siRNA (SIRT6 siRNA 1, SIRT6 siRNA 2), Investigation of the phosphorylation status of AKT, Examining PTEN expression and examining the AKT pathway while SIRT6 is silenced. To evaluate the SIRT6, phospho-AKT, AKT, and PTEN proteins, western blot was used. It was discovered that SIRT6 expression was significantly elevated in both NSCLC cells and primary lung cancers. Mechanistic research has shown that silencing SIRT6 increases AKT phosphorylation. Overall, the research demonstrated that SIRT6 downregulation induced posttranslational modification in NSCLC cell lines to control AKT/Wnt/β-catenin signaling, offering a potential biomarker and strategy for lung cancer prevention.