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Mammalian target of rapamycin complex 1 and cyclooxygenase 2 pathways cooperatively exacerbate endometrial cancer

Takiko Daikoku1, Jumpei Terakawa1, Md M Hossain2

  • 1Division of Reproductive Sciences, Perinatal Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.

The American Journal of Pathology
|July 25, 2014
PubMed

Insights

Combining celecoxib (Cox2 inhibitor) and rapamycin (mTORC1 inhibitor) effectively reduces endometrial cancer (EMC) progression. This study reveals cross-regulation between Cox2 and mTORC1 pathways in EMC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Endometrial cancer (EMC) has poorly understood causes and limited treatments for advanced stages.
  • Mutations in the phosphatase and tensin homologue gene are common in EMC.
  • Cyclooxygenase 2 (Cox2) and mammalian target of rapamycin complex 1 (mTORC1) are upregulated in EMC but their interactive roles are unclear.

Purpose of the Study:

  • To investigate the interactive roles of Cyclooxygenase 2 (Cox2) and mammalian target of rapamycin complex 1 (mTORC1) signaling in endometrial cancer (EMC) progression.
  • To explore the efficacy of combined inhibition of Cox2 and mTORC1 in EMC models.

Main Methods:

  • Utilized a Cox2 inhibitor (celecoxib) and an mTORC1 inhibitor (rapamycin).
  • Employed mouse models of EMC and human EMC cell lines.
  • Analyzed the effects of individual and combined inhibitor treatments on EMC progression and signaling pathways.

Main Results:

  • Combined treatment with celecoxib and rapamycin significantly reduced EMC progression.
  • Rapamycin treatment led to decreased Cox2 expression.
  • Celecoxib treatment resulted in reduced mTORC1 activity.
  • Demonstrated cross-regulation between Cox2 and mTORC1 signaling pathways.

Conclusions:

  • Cox2 and mTORC1 signaling pathways are cross-regulated in endometrial cancer.
  • These pathways cooperatively contribute to the exacerbation of EMC.
  • Combined inhibition of Cox2 and mTORC1 represents a potential therapeutic strategy for advanced EMC.

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