ArticleExperimental biology and medicine (Maywood, N.J.)2021
Megestrol acetate drives endometrial carcinoma cell senescence via interacting with progesterone receptor B/FOXO1 axis.
Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Pioneering preoperative anti-PD-1 immunotherapy enables curative resection in dMMR advanced/recurrent endometrial carcinoma: a case series (2020-2022).Discover oncology · 2026Article
- The gene panel with methylation-related genes and clinical factors for predicting overall survival of endometrial cancer.Journal of medical biochemistry · 2025Article
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
- Panaxatriol exerts anti-senescence effects and alleviates osteoarthritis and cartilage repair fibrosis by targeting UFL1.Journal of advanced research · 2025Article
- NK cells: shielding senescence homeostasis in the decidua during early pregnancy.Seminars in immunopathology · 2025Review
- mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes.International journal of molecular sciences · 2024Review
- DEAD-box helicase 56 functions as an oncogene promote cell proliferation and invasion in gastric cancer via the FOXO1/p21 Cip1/c-Myc signaling pathway.Bioengineered · 2022Article
- Neferine Exerts Ferroptosis-Inducing Effect and Antitumor Effect on Thyroid Cancer through Nrf2/HO-1/NQO1 Inhibition.Journal of oncology · 2022Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Megestrol acetate is a common and efficient anticancer progesterone. To explore the activity and the therapeutic mechanisms of megestrol acetate in endometrial cancer, human endometrial cancer cell lines Ishikawa and HHUA overexpressing progesterone receptor A (PR-A) and progesterone receptor B (PR-B) were treated with megestrol acetate. Cell viability, apoptosis, cycle arrest, and senescence, as well as the expressions of p21 and p16, two hallmarks of cellular senescence, were evaluated. Compared with the control, >10 nmol/L megestrol acetate treatment could significantly reduce endometrial cancer cell growth, and induce the irreversible G1 arrest and cell senescence. The expression of cyclin D1 in megestrol acetate treated cells was downregulated, while the expressions of p21 and p16 were upregulated via PR-B isoform. FOXO1 inhibitor AS1842856 could significantly abrogate megestrol acetate-induced cell senescence, suggesting that FOXO1 was involved in megestrol acetate/PR-B axis. These findings may provide a new understanding for the treatment of human endometrial cancer.
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