ArticleThe American journal of pathology2014
Mammalian target of rapamycin complex 1 and cyclooxygenase 2 pathways cooperatively exacerbate endometrial cancer.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Inflammasome activity regulation by PUFA metabolites.Frontiers in immunology · 2024Review
- In situ imaging reveals disparity between prostaglandin localization and abundance of prostaglandin synthases.Communications biology · 2021Article
- Insights Into the Regulation of Gynecological Inflammation-Mediated Malignancy by Metalloproteinases.Frontiers in cell and developmental biology · 2021Review
- COX-2-PGEArchives of gynecology and obstetrics · 2020Review
- The Role of Eicosanoids in Gynecological Malignancies.Frontiers in pharmacology · 2020Review
- Cyclooxygenase-2 and β-Catenin as Potential Diagnostic and Prognostic Markers in Endometrial Cancer.Frontiers in oncology · 2020Article
- Salt Induces Adipogenesis/Lipogenesis and Inflammatory Adipocytokines Secretion in Adipocytes.International journal of molecular sciences · 2019Article
- The uterine epithelial loss of Pten is inefficient to induce endometrial cancer with intact stromal Pten.PLoS genetics · 2018Article
- Celecoxib treatment of fibrous dysplasia (FD) in a human FD cell line and FD-like lesions in mice with protein kinase A (PKA) defects.Molecular and cellular endocrinology · 2017Article
- Celecoxib reduces glucocorticoids in vitro and in a mouse model with adrenocortical hyperplasia.Endocrine-related cancer · 2016Article
- Neutrophils Oppose Uterine Epithelial Carcinogenesis via Debridement of Hypoxic Tumor Cells.Cancer cell · 2015Article
- Activation of protein synthesis in mouse uterine epithelial cells by estradiol-17β is mediated by a PKC-ERK1/2-mTOR signaling pathway.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.