ArticleCancer letters2017
Activin A stimulates migration of the fallopian tube epithelium, an origin of high-grade serous ovarian cancer, through non-canonical signaling.
Article in Cancer letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 79 citations in OpenAlex.
- Whole-Exome Sequencing Identifies Candidate Genomic Features Associated with Response to Platinum-Based Chemotherapy and Ixabepilone-Based Treatment in Ovarian Cancer.International journal of molecular sciences · 2026Article
- Endogenous targeting lipid nanoparticles for systemic mRNA delivery to lung cancer tumors.Journal of controlled release : official journal of the Controlled Release Society · 2026Article
- Activin A-Targeted Therapy in Cancer: An Updated Review on Challenges and Opportunities in Clinical Translation.Current pharmaceutical design · 2026Review
- ACVR2A facilitates trophoblast cell invasion through TCF7/c-JUN pathway in pre-eclampsia progression.eLife · 2025Article
- Identification of oncogenes associated with colorectal cancer mortality and the effect of cinnamon-conjugated magnetic nanoparticles on their expression.Scientific reports · 2025Article
- INHBABMC cancer · 2025Article
- Prognostic Significance ofBiomedicines · 2025Article
- Review
- Targeting Metastasis in Head and Neck Squamous Cell Carcinoma Using Follistatin mRNA Lipid Nanoparticles.ACS nano · 2024Article
- COL10A1 Facilitates Prostate Cancer Progression by Interacting With INHBA to Activate the PI3K/AKT Pathway.Journal of cellular and molecular medicine · 2024Article
- Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024Review
- Activin A, a Novel Chemokine, Induces Mouse NK Cell Migration via AKT and Calcium Signaling.Cells · 2024Article
- Article
- INHBA(+) cancer-associated fibroblasts generate an immunosuppressive tumor microenvironment in ovarian cancer.NPJ precision oncology · 2024Article
- EM-transcriptomic signature predicts drug response in advanced stages of high-grade serous ovarian carcinoma based on ascites-derived primary cultures.Frontiers in pharmacology · 2024Article
- Long noncoding RNA FTX promotes epithelial-mesenchymal transition of epithelial ovarian cancer through modulating miR-7515/TPD52 and activating Met/Akt/mTOR.Histology and histopathology · 2023Article
- Evolving roles of activins and inhibins in ovarian cancer pathophysiology.American journal of physiology. Cell physiology · 2023Review
- A therapeutic target for CKD: activin A facilitates TGFβ1 profibrotic signaling.Cellular & molecular biology letters · 2023Article
- Machine learning-assisted analysis of epithelial mesenchymal transition pathway for prognostic stratification and immune infiltration assessment in ovarian cancer.Frontiers in endocrinology · 2023Article
- Nanoparticle-Based Follistatin Messenger RNA Therapy for Reprogramming Metastatic Ovarian Cancer and Ameliorating Cancer-Associated Cachexia.Small (Weinheim an der Bergstrasse, Germany) · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Factors that stimulate the migration of fallopian tube epithelial (FTE)-derived high-grade serous ovarian cancer (HGSOC) to the ovary are poorly elucidated. This study characterized the effect of the ovarian hormone, activin A, on normal FTE and HGSOC. Activin A and TGFβ1 induced an epithelial-to-mesenchymal transition in murine oviductal epithelial (MOE) cells, but only activin A increased migration. The migratory effect of activin A was independent of Smad2/3 and required phospho-AKT, phospho-ERK, and Rac1. Exogenous activin A stimulated migration of the HGSOC cell line OVCAR3 through a similar mechanism. Activin A signaling inhibitors, SB431542 and follistatin, reduced migration in OVCAR4 cells, which expressed activin A subunits (encoded by INHBA). Murine superovulation increased phospho-Smad2/3 immunostaining in the FTE. In Oncomine, transcripts for the activin A receptors (ACVR1B and ACVR2A) were higher in serous tumors relative to the normal ovary, while inhibitors of activin A signaling (INHA and TGFB3) were lower. High expression of both INHBA and ACVR2A, but not TGFβ receptors or co-receptors, was associated with shorter disease-free survival in serous cancer patients. These results suggest activin A stimulates migration of FTE-derived tumors to the ovary.
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