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Metformin inhibits cell proliferation in SKM-1 cells via AMPK-mediated cell cycle arrest

Xiaojia Zhou1, Yunchun Kuang2, Simin Liang1

  • 1Department of Hematology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Journal of Pharmacological Sciences
|November 21, 2019
PubMed

Insights

Metformin, an antidiabetic drug, inhibits proliferation in acute myeloid leukemia with myelodysplastic syndromes (AML-MDS) cells. This effect is mediated by AMPK, leading to cell cycle arrest, not apoptosis.

Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Metformin exhibits anti-cancer properties in hematological malignancies.
  • The impact of metformin on acute myeloid leukemia with myelodysplastic syndromes (AML-MDS) transformation is not well understood.

Purpose of the Study:

  • To investigate metformin's effects on the AML-MDS cell line SKM-1.
  • To elucidate the underlying molecular mechanisms of metformin's action in AML-MDS cells.

Main Methods:

  • SKM-1 cells were treated with varying metformin concentrations.
  • Cell proliferation, apoptosis, and cell cycle were analyzed using CCK-8 and flow cytometry.
  • Protein expression of cell cycle regulators and AMPK was assessed via Western blot; AMPK knockdown was performed using RNA interference.

Main Results:

  • Metformin suppressed SKM-1 cell proliferation in a dose- and time-dependent manner.
  • Metformin induced G0/G1 cell cycle arrest, with increased p-AMPK, p53, p21CIP1, and p27KIP1, and decreased CDK4 and CyclinD1.
  • AMPK knockdown diminished metformin's inhibitory effects on cell proliferation.

Conclusions:

  • Metformin inhibits proliferation of AML-MDS cells (SKM-1 line).
  • The mechanism involves AMPK-mediated G0/G1 cell cycle arrest.
  • Metformin shows potential as a therapeutic agent for AML-MDS.
Keywords:
AMPKCell cycleMetforminSKM-1 cells

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