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miR-133a-3p/FOXP3 axis regulates cell proliferation and autophagy in gastric cancer

Jia-Peng Li1, Hui-Min Zhang1, Mei-Jun Liu1

  • 1College of Life and Health Sciences, Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan, Hubei, China.

Journal of Cellular Biochemistry
|January 7, 2020
PubMed

Insights

MicroRNA miR-133a-3p and transcription factor FOXP3 influence gastric cancer (GC) cell proliferation and autophagy. Decreasing FOXP3 protein levels via miR-133a-3p boosts GC cell growth and autophagy, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Gastric cancer (GC) survival rates remain suboptimal despite advancements in treatment.
  • Understanding molecular mechanisms driving GC progression is crucial for developing effective therapies.

Purpose of the Study:

  • To investigate the roles of microRNA miR-133a-3p and transcription factor FOXP3 in gastric cancer cell proliferation and autophagy.
  • To elucidate the interaction between FOXP3, miR-133a-3p, and their impact on GC.

Main Methods:

  • Investigated the effects of FOXP3 knockdown on GC cell proliferation and autophagy.
  • Analyzed the direct binding of FOXP3 to the TP53 promoter region.
  • Examined the influence of miR-133a-3p on FOXP3 protein levels by targeting its 3'-UTR.

Main Results:

  • Knockdown of FOXP3 significantly increased proliferation and autophagy in GC cells.
  • FOXP3 was found to directly inhibit the expression of TP53.
  • miR-133a-3p was shown to upregulate GC cell proliferation and autophagy by reducing FOXP3 protein levels.

Conclusions:

  • FOXP3 plays an inhibitory role in gastric cancer cell proliferation and autophagy.
  • miR-133a-3p promotes GC progression by targeting FOXP3.
  • These findings offer novel insights into GC pathogenesis and potential therapeutic strategies.
Keywords:
FOXP3autophagygastric cancermiR-133a-3pproliferation

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