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Metformin counteracts lipid accumulation and cell proliferation in hepatocellular carcinoma via regulating

Yannan Qi1, Chuanrui Chen1, Yuwei Dai1

  • 1College of Life Sciences, Nanjing Normal University, Nanjing, China.

Cell Cycle (Georgetown, Tex.)
|May 3, 2026
PubMed

Insights

Metformin, an antidiabetic drug, inhibits liver cancer cell growth and fat buildup by altering RNA methylation. It targets the METTL3 enzyme, impacting key genes involved in lipid metabolism and cell proliferation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Metformin is a primary treatment for diabetes with observed anticancer effects.
  • The exact mechanisms of metformin's action in hepatocellular carcinoma (HCC) are not fully understood.
  • N6-methyladenosine (m6A) RNA methylation plays a role in various cellular processes, including cancer development.

Purpose of the Study:

  • To investigate the role of metformin in modulating m6A RNA methylation in HCC cells.
  • To elucidate the specific molecular pathways through which metformin affects lipid metabolism and proliferation in HCC.
  • To identify key mediators of metformin's anticancer effects in HCC.

Main Methods:

  • Treatment of HCC cell lines (HepG2, Huh7) with metformin.
  • Measurement of intracellular lipid levels (triglycerides, cholesterol) and lipid droplet accumulation.
  • Assessment of cell proliferation rates.
  • Analysis of m6A RNA methylation levels, including the expression of METTL3 and FTO.
  • Gene silencing (METTL3 knockdown) and overexpression studies.
  • Investigation of the METTL3/ACC1/FASN signaling pathway.

Main Results:

  • Metformin significantly reduced lipid accumulation and proliferation in HCC cells.
  • Metformin decreased global m6A methylation by downregulating METTL3 and upregulating FTO.
  • METTL3 overexpression reversed metformin's effects, while METTL3 knockdown mimicked them.
  • Metformin suppressed the METTL3/ACC1/FASN axis, reducing m6A modification and expression of ACC1 and FASN transcripts.

Conclusions:

  • Metformin inhibits lipid accumulation and proliferation in HCC cells via m6A RNA methylation modulation.
  • METTL3 is identified as a crucial mediator of metformin's metabolic and antiproliferative effects in HCC.
  • This study reveals a novel epitranscriptomic mechanism underlying metformin's tumor-inhibiting activity in hepatocellular carcinoma.
Keywords:
Hepatocellular carcinomaMETTL3cell proliferationlipid accumulationmetformin

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