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Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
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Published on: April 6, 2012

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MicroRNA-23a-3p influences the molecular mechanism of gastric cancer cells via CCL22/PI3K/Akt axis

Zhipeng Jiang1, Hua Chen2, Min Su3

  • 1Department of Gastrointestinal Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou City, Guangdong Province, China.

Bioengineered
|December 7, 2021
PubMed

Insights

MicroRNA-23a-3p (miR-23a-3p) is down-regulated in gastric cancer (GC), inhibiting tumor growth and progression. Restoring miR-23a-3p may offer a new therapeutic target for GC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • MicroRNAs (miRNAs) are crucial regulators in human cancers, including gastric cancer (GC).
  • The specific role of miR-23a-3p in GC pathogenesis remains largely uncharacterized.
  • Understanding miRNA functions is vital for developing novel cancer therapies.

Purpose of the Study:

  • To elucidate the functional role of miR-23a-3p in gastric cancer.
  • To investigate the molecular mechanisms underlying miR-23a-3p's action in GC.
  • To assess the prognostic significance of miR-23a-3p in GC patients.

Main Methods:

  • Analysis of miR-23a-3p expression levels in GC tissues and correlation with patient prognosis.
  • In vitro functional assays (proliferation, invasion, migration, apoptosis) to assess miR-23a-3p's effects.
  • Double luciferase reporter assays to identify miR-23a-3p targets.
  • In vivo tumor xenograft models to evaluate miR-23a-3p's efficacy.
  • Western blotting to analyze PIK3/Akt pathway activation.

Main Results:

  • miR-23a-3p was significantly down-regulated in GC tissues, correlating with poor patient prognosis.
  • Overexpression of miR-23a-3p suppressed GC cell proliferation, invasion, migration, and PIK3/Akt phosphorylation, while promoting apoptosis.
  • Knockdown of miR-23a-3p accelerated GC growth.
  • CCL22 was identified as a direct target of miR-23a-3p.
  • Functional rescue experiments confirmed CCL22 mediated miR-23a-3p's suppressive effects.
  • In vivo studies showed elevated miR-23a-3p inhibited tumor growth and CCL22/p-PIK3/Akt expression.

Conclusions:

  • miR-23a-3p acts as a tumor suppressor in gastric cancer.
  • miR-23a-3p exerts its inhibitory effects by down-regulating CCL22 and consequently blocking the PI3K/AKT signaling pathway.
  • miR-23a-3p represents a potential molecular target for the clinical treatment of gastric cancer.
Keywords:
PI3K/AKTgastric cancermiR-23a-3pmolecular mechanism

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