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Carbon source and myc expression influence the antiproliferative actions of metformin

Shiva Javeshghani1, Mahvash Zakikhani, Shane Austin

  • 1Division of Experimental Medicine, McGill University, Montreal, Quebec, Canada.

Cancer Research
|October 9, 2012
PubMed

Insights

Metformin

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Biguanides, including metformin, are being investigated for cancer prevention and treatment.
  • Metformin's known mechanism involves inhibiting oxidative phosphorylation and activating AMPK.
  • This can lead to growth inhibition or an energetic crisis depending on cellular pathways.

Purpose of the Study:

  • To investigate how different carbon sources affect metformin's impact on cancer cells.
  • To explore the role of MYC in mediating metformin sensitivity.

Main Methods:

  • Exposure of transformed cell lines to metformin in the presence or absence of glucose.
  • Measurement of cellular ATP levels and cell number.
  • Assessment of metformin sensitivity in cells with MYC overexpression.

Main Results:

  • Metformin significantly reduced ATP and cell number when glucose was absent but glutamine was present.
  • In the presence of glucose, metformin increased glycolysis, leading to only modest reductions in ATP and cell number.
  • MYC overexpression sensitized cells to metformin's antiproliferative effects, suggesting a role in "glutamine addiction".

Conclusions:

  • Metformin's effects on cancer cells are significantly influenced by the available carbon source.
  • Increased glycolysis, stimulated by glucose, can attenuate metformin's antiproliferative activity.
  • These findings highlight novel factors affecting metformin sensitivity and suggest therapeutic implications.

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