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Metformin suppresses CRC growth by inducing apoptosis via ADORA1

Bin Lan1, Jian Zhang2, Peng Zhang3

  • 1Department of gastroenterological surgery, the First Affiliated Hospital, Fujian Medical University, 20 chazhong Rd, Fuzhou 350005, Fujian Province, China, lanbin111@yahoo.com.

Frontiers in Bioscience (Landmark Edition)
|November 5, 2016
PubMed

Insights

Metformin, an anti-diabetic drug, inhibits growth and promotes apoptosis in colorectal cancer (CRC) by activating the AMPK-mTOR pathway. This effect is mediated through adenosine A1 receptor (ADORA1) upregulation, revealing metformin's anti-neoplastic potential in CRC.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Metformin, an anti-diabetic medication, shows anti-proliferative effects in various cancers.
  • The specific mechanisms of metformin in human colorectal cancer (CRC) are not well understood.

Purpose of the Study:

  • To investigate the function and molecular mechanisms of metformin in human colorectal cancer (CRC).
  • To elucidate the role of adenosine A1 receptor (ADORA1) in metformin's anti-cancer effects.

Main Methods:

  • Utilized human colorectal cancer cell lines.
  • Investigated the activation of the AMPK-mTOR pathway.
  • Assessed the expression and activity of adenosine A1 receptor (ADORA1).
  • Employed specific inhibitors to block ADORA1 activity.

Main Results:

  • Metformin induced growth inhibition and apoptosis in CRC cells via the AMPK-mTOR pathway.
  • Metformin significantly upregulated ADORA1 expression in CRC cells.
  • Inhibition of ADORA1 activity reversed the metformin-induced growth inhibition.
  • ADORA1-mediated effects of metformin were dependent on the AMPK-mTOR pathway.

Conclusions:

  • Metformin suppresses human colorectal cancer growth by inducing apoptosis.
  • The anti-cancer effects of metformin in CRC are mediated through ADORA1.
  • This study provides evidence for the anti-neoplastic effects of metformin in treating human colorectal cancer.

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