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Progesterone inhibits endometrial cancer growth by inhibiting glutamine metabolism through ASCT2

Jinqiu Guo1, Jianhui Fan1, Yaru Zhang1

  • 1Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Dalian Medical University, Dalian, China.

Bioscience Reports
|February 28, 2024
PubMed

Insights

Progesterone therapy inhibits endometrial carcinoma (EC) growth by targeting glutamine metabolism and down-regulating the ASCT2 transporter. This provides a new mechanism for EC treatment, preserving fertility in young women.

Area of Science:

  • Gynecologic Oncology
  • Cancer Metabolism
  • Endocrinology

Background:

  • Endometrial carcinoma (EC) is a prevalent gynecologic malignancy.
  • Current surgical treatments for EC do not preserve fertility in young patients.
  • Progesterone (P4) therapy is a viable fertility-sparing option for EC.

Purpose of the Study:

  • To investigate the role of glutamine metabolism in progesterone's effect on endometrial carcinoma.
  • To elucidate the mechanism by which P4 influences EC growth and fertility preservation.

Main Methods:

  • In vitro studies on EC cells to assess glutamine metabolism and ASCT2 expression.
  • In vivo xenograft models in mice to evaluate P4's effect on tumor growth.
  • Analysis of key enzymes involved in glutamine metabolism pathways.

Main Results:

  • Progesterone (P4) significantly inhibited glutamine metabolism in EC cells.
  • P4 down-regulated the expression of the glutamine transporter ASCT2, reducing glutamine uptake.
  • In vivo studies confirmed P4 inhibited tumor growth and key glutamine metabolism enzymes.

Conclusions:

  • Progesterone directly regulates glutamine metabolism in endometrial carcinoma.
  • The anticancer effects of P4 therapy in EC are mediated by ASCT2 inhibition.
  • This study provides a metabolic mechanism for P4's efficacy in fertility-sparing EC treatment.
Keywords:
ASCT2Endometrial carcinomaGlutamine metabolismProgesterone

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