TLR4 inhibited autophagy by modulating PI3K/AKT/mTOR signaling pathway in GC cell lines

Abstract

Abstract Toll-like receptors (TLRs) are pattern recognition receptors that are found on both immune cells and cancerous cells. Gastric cancer (GC) cells/tissues have been shown to exhibit elevated levels of TLR4. Here, we examined the role of TLR4 on autophagy and growth in GC cells. Real-time quantitative PCR (RT-qPCR) and western blot (WB) were used to determine TLR4 levels at different stages of GC cells/tissues as well as the levels of autophagy-related proteins (ARPs) and determine the underlying signaling mechanism. Cellular growth was assessed via the CCK-8 assay. The protein and mRNA levels of ARPs were elucidated, followed by the estimation of the involved signaling pathways. Our results demonstrated that the modulation of the PI3K/AKT/mTOR pathway resulted from autophagy inhibition/induction, which was in turn induced by the overexpression and knockdown of TLR4. Thus, TLR4 played a vital role in GC progression.