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TNFAIP8 regulates gastric cancer growth via mTOR-Akt-ULK1 pathway and autophagy signals

Zheng Chen1, Jianguo Zhang2, Chenyang Dong3

  • 1Tumor Research and Therapy Center, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.

Journal of Cellular and Molecular Medicine
|March 8, 2021
PubMed

Insights

Tumor necrosis factor-alpha-induced protein 8 (TNFAIP8) is upregulated in gastric cancer (GC). TNFAIP8 promotes GC cell viability and migration while inhibiting apoptosis and activating autophagy via the mTOR-Akt-ULK1 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Gastric cancer (GC) remains a significant global health challenge.
  • Understanding the molecular mechanisms driving GC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the role of TNFAIP8 in gastric cancer.
  • To elucidate the molecular pathways influenced by TNFAIP8 in GC cells.

Main Methods:

  • Gene expression analysis (RT-PCR, Western Blot) in GC tissues and cells.
  • In vitro studies involving gene silencing and overexpression in GC cell lines.
  • Functional assays including CCK-8, Transwell, and flow cytometry.
  • In vivo studies using nude mouse xenograft models with histological analysis (HE, IHC).

Main Results:

  • TNFAIP8 mRNA and protein levels were significantly elevated in GC tissues and cells compared to normal controls.
  • Overexpression of TNFAIP8 enhanced GC cell viability, migration, and autophagy.
  • TNFAIP8 overexpression led to decreased apoptosis and inhibition of the mTOR-Akt-ULK1 signaling pathway.
  • Tumor growth was promoted in vivo when TNFAIP8 was overexpressed.

Conclusions:

  • TNFAIP8 plays a critical role in promoting gastric cancer progression.
  • TNFAIP8 appears to exert its effects by down-regulating the mTOR-Akt-ULK1 pathway and activating autophagy.
  • Targeting TNFAIP8 may represent a potential therapeutic strategy for gastric cancer.
Keywords:
TNFAIP8autophagygastric cancermTOR-Akt-ULK1

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