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Metformin reduces the Walker-256 tumor development in obese-MSG rats via AMPK and FOXO3a

Eveline A I F de Queiroz1, Eliana H Akamine2, Maria Helena C de Carvalho2

  • 1Department of Pharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil; Department of Physiological Sciences, State University of Londrina, Londrina, Brazil.

Life Sciences
|December 16, 2014
PubMed
Abstract

Insights

Metformin may help manage obesity-related cancers. This study found metformin reduced tumor development in obese rats by affecting key cellular pathways, suggesting a potential therapeutic role.

Area of Science:

  • Oncology
  • Metabolic Syndrome
  • Pharmacology

Background:

  • Obesity is linked to increased cancer risk.
  • Metformin, an anti-diabetic drug, shows potential anti-cancer properties.

Purpose of the Study:

  • To investigate the mechanisms of obesity-driven tumor growth.
  • To analyze metformin's effect on tumor development in an obese model.

Main Methods:

  • Obesity was induced in Wistar rats using monosodium glutamate (MSG).
  • Walker-256 tumor cells were implanted, and metformin treatment was initiated.
  • Tumor development and molecular markers were analyzed in control and obese groups, with and without metformin.

Main Results:

  • Obese rats exhibited higher tumor development compared to controls.
  • Obesity-associated tumor growth involved insulin-IR-ERK1/2 pathway activation and anti-apoptotic effects.
  • Metformin reduced tumor growth in obese rats, potentially via increased pRb/p27 expression, activated AMPK/FOXO3a, and reduced p-ERK1/2.

Conclusions:

  • Obesity promotes tumor development through specific molecular pathways.
  • Metformin counteracts obesity's stimulatory effect on tumor growth.
  • Metformin demonstrates potential as an adjunct therapy for managing obesity-related cancers.
Keywords:
AMPKApoptosisBreast cancerFOXO3aMetformin

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