ArticleOncotarget2017
Overactive mTOR signaling leads to endometrial hyperplasia in aged women and mice.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- Extracellular matrix: new insights into its role in female reproductive aging and potential therapeutic strategies.npj aging · 2026Review
- Evolutionary perspectives on endometrial cancer: antagonistic pleiotropy.Molecular & cellular oncology · 2026Review
- The Nexus of Iron, Senescence, and Fibrosis in Endometriosis: A Narrative Review.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Rapamycin inhibits tamoxifen-induced endometrial proliferation in vitro as a pilot approach for endometrial protection in breast cancer.Scientific reports · 2025Article
- Uterine Aging and Reproduction: Dealing with a Puzzle Biologic Topic.International journal of molecular sciences · 2023Review
- MIG-6 Is Critical for Progesterone Responsiveness in Human Complex Atypical Hyperplasia and Early-Stage Endometrial Cancer.International journal of molecular sciences · 2022Article
- The Role of mTOR and eIF Signaling in Benign Endometrial Diseases.International journal of molecular sciences · 2022Review
- Current and Future Roles of Circular RNAs in Normal and Pathological Endometrium.Frontiers in endocrinology · 2021Review
- Epidemiological aspects of the outcomes from the treatment of endometriosis: Experience from two different geographical areas.Experimental and therapeutic medicine · 2020Article
- Article
- Identification of a Goat Intersexuality-Associated Novel Variant Through Genome-Wide Resequencing and Hi-C.Frontiers in genetics · 2020Article
- Mechanistic target of rapamycin signaling in mouse models of accelerated aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2020Review
- Review
- VEGF-mTOR signaling links obesity and endometrial cancer.Oncoscience · 2018Article
- Targeting ROR1 inhibits epithelial to mesenchymal transition in human lung adenocarcinoma via mTOR signaling pathway.International journal of clinical and experimental pathology · 2018Article
- Article
- Age-related mTOR in gynaecological cancers.Aging · 2017Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
During aging, uncontrolled epithelial cell proliferation in the uterus results in endometrial hyperplasia and/or cancer development. The mTOR signaling pathway is one of the major regulators of aging as suppression of this pathway prolongs lifespan in model organisms. Genetic alterations in this pathway via mutations and/or amplifications are often encountered in endometrial cancers. However, the exact contribution of mTOR signaling and uterine aging to endometrial pathologies is currently unclear. This study examined the role of mTOR signaling in uterine aging and its implications in the development of endometrial hyperplasia. The hyperplastic endometrium of both postmenopausal women and aged mice exhibited elevated mTOR activity as seen with increased expression of the pS6 protein. Analysis of uteri from Pten heterozygous and Pten overexpressing mice further confirmed that over-activation of mTOR signaling leads to endometrial hyperplasia. Pharmacological inhibition of mTOR signaling using rapamycin treatment suppressed endometrial hyperplasia in aged mice. Furthermore, treatment with mTOR inhibitors reduced colony size and proliferation of a PTEN negative endometrial cancer cell line in 3D culture. Collectively, this study suggests that hyperactivation of the mTOR pathway is involved in the development of endometrial hyperplasia in aged women and mice.
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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.