ArticleOncoTargets and therapy2017
PI3K/AKT/mTOR pathway promotes progestin resistance in endometrial cancer cells by inhibition of autophagy.
Article in OncoTargets and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 80 citations in OpenAlex.
- Review
- Obesity, Bariatric Surgery, and Cancer Risk: Nutritional Perspectives and Long-Term Clinical Implications.Nutrients · 2026Review
- Autophagy modulation in gynaecologic oncology: insights into immune regulation and therapeutic potential.Frontiers in immunology · 2026Review
- Advances in the molecular mechanisms underlying progestin resistance in endometrial cancer.Fundamental research · 2025Review
- Oncological safety and fertility outcomes of controlled ovarian stimulation in patients with early-stage endometrial cancer.F&S reports · 2025Article
- miR-21 regulates autophagy and apoptosis of ectopic endometrial stromal cells of adenomyosis via PI3K/ AKT/ mTOR pathway.Scientific reports · 2025Article
- Anticancer Drug Discovery from Natural Compounds Targeting PI3K/AKT/mTOR Signaling Pathway.Current medicinal chemistry · 2025Review
- IKBKE modulates autophagy and progestin resistance in endometrial cancer.Frontiers in oncology · 2025Article
- Krüppel-like factor 12 decreases progestin sensitivity in endometrial cancer by inhibiting the progesterone receptor signaling pathway.Translational oncology · 2024Article
- Structure-based pharmacophore modeling and DFT studies of Indian Ocean-derived red algal compounds as PI3Kα inhibitors.Molecular diversity · 2024Article
- Focusing on the role of protein kinase mTOR in endometrial physiology and pathology: insights for therapeutic interventions.Molecular biology reports · 2024Review
- The effect of lipidomes on the risk of endometrioid endometrial cancer: a Mendelian randomization study.Frontiers in oncology · 2024Article
- Copper homeostasis and cuproptosis in gynecological cancers.Frontiers in cell and developmental biology · 2024Review
- Advances in research on autophagy mechanisms in resistance to endometrial cancer treatment.Frontiers in oncology · 2024Review
- New insights for gynecological cancer therapies: from molecular mechanisms and clinical evidence to future directions.Cancer metastasis reviews · 2023Review
- Verteporfin reverses progestin resistance through YAP/TAZ-PI3K-Akt pathway in endometrial carcinoma.Cell death discovery · 2023Article
- Effect of integrin α7 on cell proliferation, invasion, apoptosis and the PI3K/AKT pathway, and its association with clinicopathological features in endometrial cancer.Oncology letters · 2023Article
- Analysis of some flavonoids for inhibitory mechanism against cancer target phosphatidylinositol 3-kinase (PI3K) using computational tool.Frontiers in pharmacology · 2023Article
- LncRNAs signatures associated with cuproptosis predict the prognosis of endometrial cancer.Frontiers in genetics · 2023Article
- ABX-1431 inhibits the development of endometrial adenocarcinoma and reverses progesterone resistance by targeting MGLL.Cell death & disease · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is now one of the most common malignant tumors in young women. In all, 90% of young patients with EC have a high expression of progesterone recep tor, can be treated with progestin, and have very good prognosis. However, some of the young EC patients are resistant to progestin, the mechanism of which is unclear. To illuminate the mechanism by which endometrial cells acquire progestin resistance, we treated Ishikawa cells by slowly increasing dosage of progestin and established a progestin-resistant cell subline. We show here that progesterone resistant cells acquire increased proliferation rate and interestingly decreased autophagy. To uncover the mechanism by which cells increase proliferation and bypass autophagy, we found higher activation of phosphatidylinositol 3-kinase/AKT/mTOR signaling pathway was necessary to this malignant acquirement by RNAi technique. Further, we elucidated that activation of mTOR was sufficient and necessary for progestin resistance. RAD001, an inhibitor of mTOR, decreased phosphorylation of mTOR and inhibited proliferation of progestin-resistant cancer cells by promoting autophagy. Thus, our results indicated that mTOR can be a target to treat the progestin-resistant EC.
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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.