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

被引:2
|
作者
Zhang, Qian [1 ]
Dan, Jun [2 ]
Meng, Shuang [1 ]
Li, Yingjie [1 ]
Li, Jing [1 ]
机构
[1] Jinzhou Med Univ, Dept Gastroenterol, Affiliated Hosp 1, Jinzhou 121000, Liaoning, Peoples R China
[2] Jinzhou Med Univ, Dept Geriatr, Affiliated Hosp 1, Jinzhou 121000, Liaoning, Peoples R China
关键词
Gastric cancer; TLR4; PI3K; AKT; Autophagy; Proliferation; TOLL-LIKE RECEPTORS; EXPRESSION; TUMOR; PROMOTES; INFLAMMATION; MECHANISM; INFECTION; CARCINOMA; ADHESION; INVASION;
D O I
10.1016/j.gene.2023.147520
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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.
引用
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页数:10
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