ArticleReproductive sciences (Thousand Oaks, Calif.)2025
17beta-estradiol (E2) Regulates Malignancies and Stemness in Endometrial Carcinoma (EC) via Interacting with ESR1.
Article in Reproductive sciences (Thousand Oaks, Calif.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Network toxicology and bioinformatic investigation of the association between Bisphenol A and endometrial cancer.Scientific reports · 2026Article
- The estrogen-ferroptosis axis in postmenopausal osteoporosis, osteoarthritis, and intervertebral disc degeneration: shared mechanisms and emerging evidence.Frontiers in immunology · 2026Review
- Investigation of the mechanism of euphornin against cervical cancer using network pharmacology.Scientific reports · 2025Article
- Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer is one of the most common and fatal gynaecologic malignancies and is associated with the presence of estrogen. Endometrial cancer stem-like cells (ECSCs) are stem-like cell subpopulations endowed with self-renewal and differentiation capacities and are critical for EC progression. However, it is still unknown whether estrogen is involved in regulating stemness in EC and contributes to malignancies. Therefore, we investigated the regulatory effects of E2 treatment on oestrogen receptor-1 (ESR1).ESR1 expression was measured in EC tissues; After ESR1 overexpression of knockdown, the effects of E2 treatment was evaluated, including cell proliferation, sphere formation, invasion and colony formation. Our results indicate that ESR1 is critical for the regulatory effect of E2 on EC cells. After being cultured in serum-free medium, the ECSCs were found to be enriched in stemness markers, including CD133, CD44 and ALDH1. Interestingly, enriched ECSCs presented significantly lower expression levels of these factors than the parental cells. Overexpression of ESR1 slightly affected stemness and malignant potential in ECSCs, and the addition of 2 nM E2 markedly decreased stemness and inhibited malignant behaviours of ECSCs, including proliferation, invasion and tumour formation, in soft agar. Moreover, the addition of E2 significantly inhibited the expression of epithelial-mesenchymal transition (EMT) markers, including ZEB1, ZEB2, and E-cadherin.ESR1 is critical for regulating EC progression in the presence of E2, partially by regulating stemness in ECSCs, indicating that ESR1 might be a potential therapeutic target for EC.
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