ArticleInternational journal of oncology2021
Anti-Müllerian hormone concentration regulates activin receptor-like kinase-2/3 expression levels with opposing effects on ovarian cancer cell survival.
Article in International journal of oncology, 2021. 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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4 citing papers in PubMed, 5 citations in OpenAlex.
- Molecular mechanisms and multi-organ regulatory roles of anti-Müllerian hormone in female reproduction.Communications biology · 2026Review
- AMH and Kisspeptin Receptor Expression in Rare Hydropic Leiomyoma: A Case Study.The American journal of case reports · 2025Article
- Anti-Müllerian hormone: biology and role in endocrinology and cancers.Frontiers in endocrinology · 2024Review
- Bone morphogenetic protein signaling is a possible therapeutic target in gynecologic cancer.Cancer science · 2023Review
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Authors and funding
16 authors at 8 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Anti‑Müllerian hormone (AMH) type II receptor (AMHRII) and the AMH/AMHRII signaling pathway are potential therapeutic targets in ovarian carcinoma. Conversely, the role of the three AMH type I receptors (AMHRIs), namely activin receptor‑like kinase (ALK)2, ALK3 and ALK6, in ovarian cancer remains to be clarified. To determine the respective roles of these three AMHRIs, the present study used four ovarian cancer cell lines (COV434‑AMHRII, SKOV3‑AMHRII, OVCAR8, KGN) and primary cells isolated from tumor ascites from patients with ovarian cancer. The results demonstrated that ALK2 and ALK3 may be the two main AMHRIs involved in AMH signaling at physiological endogenous and supraphysiological exogenous AMH concentrations, respectively. Supraphysiological AMH concentrations (25 nM recombinant AMH) were associated with apoptosis in all four cell lines and decreased clonogenic survival in COV434‑AMHRII and SKOV3‑AMHRII cells. These biological effects were induced via ALK3 recruitment by AMHRII, as ALK3‑AMHRII dimerization was favored at increasing AMH concentrations. By contrast, ALK2 was associated with AMHRII at physiological endogenous concentrations of AMH (10 pM). Based on these results, tetravalent IgG1‑like bispecific antibodies (BsAbs) against AMHRII and ALK2, and against AMHRII and ALK3 were designed and evaluated.
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