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

First Author  Daikoku T Year  2014
Journal  Am J Pathol Volume  184
Issue  9 Pages  2390-402
PubMed ID  25058027 Mgi Jnum  J:213943
Mgi Id  MGI:5586925 Doi  10.1016/j.ajpath.2014.05.023
Citation  Daikoku T, et al. (2014) Mammalian target of rapamycin complex 1 and cyclooxygenase 2 pathways cooperatively exacerbate endometrial cancer. Am J Pathol 184(9):2390-402
abstractText  The underlying causes of endometrial cancer (EMC) are poorly understood, and treatment options for patients with advanced stages of the disease are limited. Mutations in the phosphatase and tensin homologue gene are frequently detected in EMC. Cyclooxygenase 2 (Cox2) and mammalian target of rapamycin complex 1 (mTORC1) are known downstream targets of the phosphatase and tensin homologue protein, and their activities are up-regulated in EMC. However, it is not clear whether Cox2 and mTORC1 are crucial players in cancer progression or whether they work in parallel or cooperatively. In this study, we used a Cox2 inhibitor, celecoxib, and an mTORC1 inhibitor, rapamycin, in mouse models of EMC and in human EMC cell lines to explore the interactive roles of Cox2 and mTORC1 signaling. We found that a combined treatment with celecoxib and rapamycin markedly reduces EMC progression. We also observed that rapamycin reduces Cox2 expression, whereas celecoxib reduces mTORC1 activity. These results suggest that Cox2 and mTORC1 signaling is cross-regulated and cooperatively exacerbate EMC.
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