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miR-496 inhibits proliferation via LYN and AKT pathway in gastric cancer

Rui Su1, Enhong Zhao1, Jun Zhang2

  • 1Department of Gastrointestinal Surgery, Affiliated Hospital of Chengde Medical College, 067000, Chengde, China.

Open Medicine (Warsaw, Poland)
|September 13, 2021
PubMed

Insights

MicroRNA-496 (miR-496) acts as a tumor suppressor in gastric cancer by inhibiting cell proliferation and metastasis. It targets Lyn kinase (LYN), impacting the AKT/mTOR pathway for potential targeted therapy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • MicroRNAs (miRNAs) are crucial regulators of cellular processes, with roles as tumor suppressors or oncogenes.
  • Gastric cancer progression involves dysregulation of cell proliferation, metastasis, and apoptosis.
  • Understanding specific miRNA functions, like miR-496, is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the functional role and underlying mechanism of miR-496 in human gastric cancer cells.
  • To determine if miR-496 acts as a tumor suppressor in gastric cancer.
  • To elucidate the molecular targets and signaling pathways affected by miR-496.

Main Methods:

  • Quantitative real-time PCR to assess miR-496 expression levels in gastric cancer cell lines (AGS, MKN45) and a normal cell line (GES-1).
  • Transfection of miR-496 mimics into AGS cells to evaluate effects on proliferation, migration, invasion, and apoptosis.
  • Western blotting to analyze protein expression levels (Bax, Active Caspase 3, Bcl-2, Total Caspase 3, LYN, AKT, mTOR).
  • Bioinformatics analysis to predict potential miR-496 targets, followed by experimental validation of LYN as a target.
  • Overexpression of LYN to assess its impact on miR-496-mediated effects and AKT/mTOR signaling.

Main Results:

  • miR-496 was significantly downregulated in gastric cancer cell lines (AGS, MKN45) compared to normal GES-1 cells.
  • Transfection with miR-496 mimics suppressed proliferation, migration, and invasion of AGS cells.
  • miR-496 mimics induced apoptosis by upregulating Bax and Active Caspase 3, and downregulating Bcl-2 and Total Caspase 3.
  • Bioinformatics and experimental data confirmed LYN as a direct target of miR-496.
  • LYN overexpression counteracted the inhibitory effects of miR-496 on tumor cell growth and the AKT/mTOR signaling pathway.

Conclusions:

  • miR-496 functions as a tumor suppressor in gastric cancer.
  • miR-496 inhibits gastric cancer cell proliferation, migration, invasion, and promotes apoptosis.
  • The tumor-suppressive activity of miR-496 is mediated through the inhibition of the LYN/AKT/mTOR signaling pathway.
  • miR-496 represents a potential biomarker for diagnosis and a therapeutic target for gastric cancer.
Keywords:
3ʹ-UTRAKT/mTOR signaling pathwayapoptosisbinding sitemiR-496

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