ArticleCancer cell international2018
Increased ETV4 expression correlates with estrogen-enhanced proliferation and invasiveness of cholangiocarcinoma cells.
Article in Cancer cell international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- ETV4/ALYREF-mediated glycolytic metabolism through PKM2 enhances resistance to ferroptosis and promotes the development of intrahepatic cholangiocarcinoma.Cancer & metabolism · 2025Article
- Applications of 3D models in cholangiocarcinoma.Frontiers in oncology · 2025Review
- Single-cell sequencing combined with machine learning to identify glioma biomarkers and therapeutic targets.Frontiers in oncology · 2025Article
- Prognostic value ofWorld journal of gastrointestinal oncology · 2024Article
- Biological effect of ETV4 and the underlying mechanism of its regulatory effect on epithelial‑mesenchymal transition in intrahepatic cholangiocarcinoma cells.Oncology letters · 2024Article
- Therapeutic Implications of Ceritinib in Cholangiocarcinoma beyond ALK Expression and Mutation.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Secular trends of intrahepatic cholangiocarcinoma in a high endemic area: A population-based study.World journal of gastroenterology · 2022Article
- Modification of STIM2 by mAnnals of translational medicine · 2022Article
- The Heparanase Regulatory Network in Health and Disease.International journal of molecular sciences · 2021Review
- E26 transformation-specific variant 4 as a tumor promotor in human cancers through specific molecular mechanisms.Molecular therapy oncolytics · 2021Review
- Drivers and suppressors of triple-negative breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Overexpression of microRNA-29b inhibits epithelial-mesenchymal transition and angiogenesis of colorectal cancer through the ETV4/ERK/EGFR axis.Cancer cell international · 2021Article
- ETV4 Is Necessary for Estrogen Signaling and Growth in Endometrial Cancer Cells.Cancer research · 2020Article
- Review
- Function and regulation of the PEA3 subfamily of ETS transcription factors in cancer.American journal of cancer research · 2020Review
- [E26 transformation-specific variant 4 promotes sorafenib and cisplatin resistance in hepatocellular carcinoma cellsNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- The Importance of CYP19A1 in Estrogen Receptor-Positive Cholangiocarcinoma.Hormones & cancer · 2018Article
- Imbalanced expression pattern of steroid receptor coactivator-1 and -3 in liver cancer compared with normal liver: An immunohistochemical study with tissue microarray.Oncology letters · 2018Article
Corrections and comments
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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
backgroundCholangiocarcinoma (CCA) is one of the worst prognosis cancer. The survival time of CCA patients is related to serum estrogen levels and estrogen has been found to enhance the proliferation and invasiveness of CCA cells in vitro. This has led to the suggestion that estrogen may play an important role in the progression of CCA. This study tests the relevance of the previous in vitro findings in vivo using a mouse xenograft model of CCA, and investigates possible signaling mechanisms involved.
methodsKKU-213 and KKU-139 CCA cell lines were used in the experiments, xenografted to nude mice and treated with a potent estrogenic agent, 17β-estradiol (E2), and/or with tamoxifen (TAM), an estrogen antagonist.
resultsThe results demonstrated that E2 could accelerate growth of the xenograft-tumor and the effect was inhibited by TAM. PCR array screening of E2 responsive genes suggested ETV4 as a promising candidate intracellular mediator. ETV4-knockdown CCA cells were generated and these showed a diminished responsiveness to E2 in both cell and spheroid proliferation assays, and in invasion tests. These results point to ETV4 as a possible mediator of E2-activated CCA progression and as a potential target of TAM-mediated inhibition.
conclusionsFinally, TAM may be suggested as an adjunctive treatment of CCA to improve the conventional cytotoxic method with more patient toleration.
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