TLR4 inhibited autophagy by modulating PI3K/AKT/mTOR signaling pathway in Gastric cancer cell lines.

• TLR4 plays a vital role in GC pathogenesis, immune response, proliferation, migration, and progression. • TLR4 expression levels are elevated in GC cell lines and tissues compared to normal tissue and cell line. • Overexpression of TLR4 promoted GC cells proliferation, inhibited cells autophagy. • The autophagy is modulating by PI3K/AKT/mTOR cellular signaling pathway in GC cell lines. Toll-like receptors (TLRs) are pattern recognition receptors found on both immune 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 proliferation in GC cells. Real-time quantitative polymerase chain reaction (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. Proliferation was assessed via the CCK-8 assay. The protein and mRNA levels of ARPs were elucidated, followed by estimating the involved signaling pathways. Our results demonstrated that the modulation of the PI3K/AKT/mTOR pathway resulted from autophagy inhibition/induction, which was induced by the overexpression and knockdown of TLR4. Thus, TLR4 played a vital role in GC progression. [ABSTRACT FROM AUTHOR]