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Metformin down-regulates endometrial carcinoma cell secretion of IGF-1 and expression of IGF-1R

Yu Zhang1, Meng-Xiong Li, Huan Wang

  • 1Department of Gynecology The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, PR China E-mail : zhyuchenchen@163.com, tigerlee777@163.com.

Asian Pacific Journal of Cancer Prevention : APJCP
|February 3, 2015
PubMed

Insights

Metformin reduces insulin-like growth factor-1 (IGF-1) secretion and insulin-like growth factor-1 receptor (IGF-1R) expression in endometrial carcinoma (EC) cells. This deactivates the PI-3K/Akt pathway, inhibiting EC cell growth.

Area of Science:

  • Oncology
  • Endocrinology
  • Molecular Biology

Background:

  • Endometrial carcinoma (EC) exhibits active insulin growth factor (IGF) system signaling.
  • Metformin is known to inhibit endometrial carcinoma cell proliferation.

Purpose of the Study:

  • To investigate the effect of metformin on IGF-1 secretion and IGF-1 receptor (IGF-1R) expression in EC cells.
  • To explore the impact of metformin on the IGF-1/IGF-1R axis and downstream signaling pathways in EC.

Main Methods:

  • Measurement of serum IGF-1 levels in EC patients and controls.
  • Assessment of IGF-1 levels in the culture medium of EC cells treated with metformin.
  • Immunohistochemical analysis of IGF-1R expression in EC tissues.
  • Evaluation of IGF-1R and p-Akt/Akt expression in metformin-treated EC cells.

Main Results:

  • Serum IGF-1 levels did not differ significantly between EC patients and controls.
  • Metformin treatment significantly decreased IGF-1 levels in the culture medium of EC cells.
  • High IGF-1R expression was observed in human endometrial carcinoma tissues.
  • Metformin treatment led to down-regulation of IGF-1R and p-Akt/Akt expression in EC cells.

Conclusions:

  • Metformin reduces IGF-1 secretion and IGF-1R expression in Ishikawa and JEC EC cell lines.
  • Metformin deactivates the PI-3K/Akt signaling pathway, contributing to the inhibition of endometrial carcinoma cell growth.

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