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

Automated summary

This study investigated the role of Toll-like receptor 4 (TLR4) in autophagy and proliferation in gastric cancer (GC) cells. The levels of TLR4 were determined in different stages of GC cells/tissues using RT-qPCR and WB, along with the levels of autophagy-related proteins (ARPs) and the underlying signaling mechanism. Proliferation was assessed using the CCK-8 assay. The results revealed that modulation of the PI3K/AKT/mTOR pathway was induced by the overexpression and knockdown of TLR4, leading to inhibition/induction of autophagy, and TLR4 played a vital role in GC progression.