ArticleNeoplasia (New York, N.Y.)2014
Elevated estrogen receptor-α in VHL-deficient condition induces microtubule organizing center amplification via disruption of BRCA1/Rad51 interaction.
Article in Neoplasia (New York, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- A New Class of BRCA1 Mimetics for ERα-Positive Breast Cancer Therapy: Design, Synthesis, In Silico Screening, In Vitro Assay, and Gene Expression Analysis.Life (Basel, Switzerland) · 2025Article
- Cysteine Cathepsins Inhibition Affects Their Expression and Human Renal Cancer Cell Phenotype.Cancers · 2020Article
- Correlation Between von Hippel-Lindau Gene Expression and Tumor SUVmax and Survival Prognosis in Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Oestrogen receptor negativity in breast cancer: a cause or consequence?Bioscience reports · 2016Review
- Cellular effects induced by 17-β-estradiol to reduce the survival of renal cell carcinoma cells.Journal of biomedical science · 2016Article
- Prevention effect of rare ginsenosides against stress-hormone induced MTOC amplification.Oncotarget · 2016Article
- Functional Studies on Primary Tubular Epithelial Cells Indicate a Tumor Suppressor Role of SETD2 in Clear Cell Renal Cell Carcinoma.Neoplasia (New York, N.Y.) · 2016Article
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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
Since loss of VHL is frequently detected early phase genetic event in human renal cell carcinoma, pVHL is assumed to be indispensable for suppression of tumor initiation step. However, induction of HIF-1α, target of pVHL E3 ligase, is more adequate to angiogenesis step after tumor mass formation. Concerning this, it has been reported that pVHL is involved in centrosome location during metaphase and regulates ER-α signaling. Here, we provide the evidences that pVHL-mediated ER-α suppression is critical for microtubule organizing center (MTOC) maintaining and elevated ER-α promotes MTOC amplification through disruption of BRCA1-Rad51 interaction. In fact, numerous MTOC in VHL- or BRCA1-deficient cells are reduced by Fulvestrant, inhibitor of ER-α expression as well as antagonist. In addition, we reveal that activation of ER signaling can increase γ-tubulin, core factor of TuRC and render the resistance to Taxol. Thus, Fulvestrant but not Tamoxifen, antagonist against ER-α, can restore the Taxol sensitivity in VHL- or BRCA1-deficient cells. Our results suggest that pVHL-mediated ER-α suppression is important for regulation of MTOC as well as drug resistance.
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