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

Qian Zhang1, Jun Dan2, Shuang Meng1

  • 1Department of Gastroenterology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning Province 121000, China.

Gene
|May 31, 2023
PubMed

Insights

Toll-like receptor 4 (TLR4) significantly impacts gastric cancer (GC) progression by influencing cell proliferation and autophagy. Targeting TLR4 and the PI3K/AKT/mTOR pathway offers potential therapeutic strategies for GC.

Area of Science:

  • Immunology
  • Oncology
  • Cell Biology

Background:

  • Toll-like receptors (TLRs) are crucial pattern recognition receptors involved in immune responses.
  • Elevated Toll-like receptor 4 (TLR4) expression is observed in gastric cancer (GC) tissues.
  • The specific role of TLR4 in GC cell autophagy and proliferation remains to be fully elucidated.

Purpose of the Study:

  • To investigate the function of TLR4 in regulating autophagy and proliferation in gastric cancer cells.
  • To determine the correlation between TLR4 levels and autophagy-related proteins (ARPs) in GC.
  • To identify the signaling pathways influenced by TLR4 in GC progression.

Main Methods:

  • Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot (WB) were employed to quantify TLR4 and ARP levels.
  • Cell Counting Kit-8 (CCK-8) assay was utilized to assess GC cell proliferation.
  • Analysis of the PI3K/AKT/mTOR signaling pathway was conducted.

Main Results:

  • TLR4 overexpression and knockdown modulated autophagy, impacting the PI3K/AKT/mTOR pathway.
  • Changes in TLR4 levels were correlated with alterations in ARP expression.
  • TLR4 significantly influenced GC cell proliferation.

Conclusions:

  • TLR4 plays a critical role in gastric cancer progression by regulating autophagy and proliferation.
  • The PI3K/AKT/mTOR pathway is implicated in TLR4-mediated effects on GC.
  • Modulating TLR4 presents a potential therapeutic avenue for gastric cancer treatment.
Keywords:
AutophagyGastric cancerPI3K/AKTProliferationTLR4

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