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Insulin-Like Growth Factor 1/Mammalian Target of Rapamycin and AMP-Activated Protein Kinase Signaling Involved in the Effects of Metformin in the Human Endometrial Cancer
  1. Dongge Cai, MD,
  2. Hongli Sun, MD,
  3. Yanhua Qi, MD,
  4. Xiaogui Zhao,
  5. Minjuan Feng, MD and
  6. Xiaoling Wu, PhD
  1. * Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Xi’an Jiaotong University;
  2. Shaanxi Institute of Pediatric Diseases, The Affiliated Children’s hospital of Xi’an Jiaotong University; and
  3. Department of Ultrasound, The Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi, People’s Republic of China.
  1. Address correspondence and reprint requests to Xiaoling Wu, MD, Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Xi’an Jiaotong University, No.157 West Fifth Road of Xi’an, Shaanxi 710004, People’s Republic of China. E-mail: yongyy123{at}yeah.net.

Abstract

Background Metformin is a well-tolerated biguanide drug used for decades to treat type 2 diabetes mellitus. In recent years, long-term administration of metformin has been found to reduce carcinogenic risk for cancers derived from various tissues. However, its cellular and molecular mechanisms of anticancer action in the endometrial cancer (EC) have not yet been fully elucidated.

Patients and Methods Sixty patients diagnosed as endometrial carcinoma were grouped into (n = 30) and non-treatment mixed (n = 30) for analysis. Thirty healthy donors are control groups. We attempt to investigate the interaction of metformin, insulin-like growth factor 1 (IGF-1) expression, and phosphorylated mammalian target of rapamycin (p-mTOR) and AMP-activated protein kinase (p-AMPK).

Results We found that high IGF-1 plasma concentrations in women with EC were reversed by conventional antidiabetic doses of metformin in the present work. In parallel, the activation of AMPK and suppression of mTOR seemed to play an important role for the effect of metformin in patients with EC.

Conclusions This pilot trial presents biological evidence consistent with antiproliferative effects of metformin in women with EC in the clinical setting.

  • Endometrial cancer
  • Metformin
  • IGF-1
  • mTOR
  • AMPK

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Footnotes

  • The authors declare no conflicts of interest.

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