自噬
PI3K/AKT/mTOR通路
生物
蛋白激酶B
TLR4型
信号转导
细胞生物学
受体
Toll样受体
免疫印迹
基因敲除
RPTOR公司
癌症研究
细胞凋亡
先天免疫系统
基因
生物化学
作者
Qian Zhang,Jun Dan,Shuang Meng,Yingjie Li,Jing Li
出处
期刊:Gene
[Elsevier]
日期:2023-05-29
卷期号:876: 147520-147520
被引量:2
标识
DOI:10.1016/j.gene.2023.147520
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.
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