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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Metformin inhibits HaCaT cell viability via the miR-21/PTEN/Akt signaling pathway

Yue Deng1, Weiyuan Ma2

  • 1Hypertension Center of Fuwai Hospital, State Key Laboratory of Cardiovascular Disease, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100006, P.R. China.

Molecular Medicine Reports
|December 30, 2017
PubMed

Insights

Metformin inhibits human skin keratinocyte (HaCaT) cell growth by downregulating microRNA-21 (miR-21). This mechanism involves increased PTEN and decreased Akt protein levels, suggesting metformin

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Metformin exhibits preclinical anti-proliferative effects on solid tumors.
  • The precise molecular mechanisms underlying metformin's anti-tumor activity require further elucidation.
  • The microRNA-21 (miR-21)/phosphatase and tensin homolog (PTEN)/AKT serine/threonine kinase 1 (Akt) pathway is a potential mediator of metformin's effects.

Purpose of the Study:

  • To investigate metformin's impact on HaCaT cell viability.
  • To explore the role of the miR-21/PTEN/Akt signaling pathway in metformin's mechanism of action.
  • To determine if modulating miR-21 affects metformin's anti-proliferative effects.

Main Methods:

  • Cell Counting Kit-8 assays for cell viability assessment.
  • Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) for miR-21 expression analysis.
  • Western blotting to quantify PTEN and Akt protein levels.
  • Transfection with a miR-21 inhibitor to manipulate miR-21 levels.

Main Results:

  • Metformin suppressed HaCaT cell growth in a dose- and time-dependent manner.
  • Metformin treatment led to a significant downregulation of miR-21 expression.
  • Inhibition of miR-21 significantly reduced HaCaT cell growth.
  • Reduced miR-21 levels correlated with increased PTEN and decreased Akt protein expression.

Conclusions:

  • Metformin effectively inhibits HaCaT cell proliferation.
  • The miR-21/PTEN/Akt signaling pathway plays a significant role in metformin's anti-proliferative mechanism.
  • These findings offer insights into metformin's potential as an anti-cancer agent.
Keywords:
HaCaT cellmetforminmiR-21PTEN/Akt

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