ArticleOncotarget2017
SHARPIN stabilizes estrogen receptor α and promotes breast cancer cell proliferation.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Decoding estrogen receptor and GPER biology: structural insights and therapeutic advances in ERα-positive breast cancer.Frontiers in oncology · 2025Review
- Article
- Mechanisms underlying linear ubiquitination and implications in tumorigenesis and drug discovery.Cell communication and signaling : CCS · 2023Review
- Stabilization of estrogen receptor α by USP37 contributes to the progression of breast cancer.Cancer science · 2023Article
- SHARPIN: Role in Finding NEMO and in Amyloid-Beta Clearance and Degradation (ABCD) Pathway in Alzheimer's Disease?Cellular and molecular neurobiology · 2022Review
- FKBP52 and FKBP51 differentially regulate the stability of estrogen receptor in breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- TRIM3 facilitates estrogen signaling and modulates breast cancer cell progression.Cell communication and signaling : CCS · 2022Article
- Decoding the Therapeutic Implications of the ERα Stability and Subcellular Distribution in Breast Cancer.Frontiers in endocrinology · 2022Review
- Calcineurin regulates the stability and activity of estrogen receptor α.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- MINDY1 promotes breast cancer cell proliferation by stabilizing estrogen receptor α.Cell death & disease · 2021Article
- SHARPIN regulates the development of clear cell renal cell carcinoma by promoting von Hippel-Lindau protein ubiquitination and degradation.Cancer science · 2021Article
- ZNF213 negatively controls triple negative breast cancer progression via Hippo/YAP signaling.Cancer science · 2021Article
- USP35, regulated by estrogen and AKT, promotes breast tumorigenesis by stabilizing and enhancing transcriptional activity of estrogen receptor α.Cell death & disease · 2021Article
- OTUD7B stabilizes estrogen receptor α and promotes breast cancer cell proliferation.Cell death & disease · 2021Article
- SOX13/TRIM11/YAP axis promotes the proliferation, migration and chemoresistance of anaplastic thyroid cancer.International journal of biological sciences · 2021Article
- Regulation of ERα Stability and Estrogen Signaling in Breast Cancer by HOIL-1.Frontiers in oncology · 2021Article
- ZNF213 Facilitates ER Alpha Signaling in Breast Cancer Cells.Frontiers in oncology · 2021Article
- TRIM11 promotes breast cancer cell proliferation by stabilizing estrogen receptor α.Neoplasia (New York, N.Y.) · 2020Article
- Regulation of Hippo signaling and triple negative breast cancer progression by an ubiquitin ligase RNF187.Oncogenesis · 2020Article
- SHARPIN Inhibits Esophageal Squamous Cell Carcinoma Progression by Modulating Hippo Signaling.Neoplasia (New York, N.Y.) · 2020Article
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptor α is expressed in the majority of breast cancers and promotes estrogen-dependent cancer progression. In our study, we identified the novel E3 ubiquitin ligase SHARPIN function to facilitate ERα signaling. SHARPIN is highly expressed in human breast cancer and correlates with ERα protein level by immunohistochemistry. SHARPIN expression level correlates with poor prognosis in ERα positive breast cancer patients. SHARPIN depletion based RNA-sequence data shows that ERα signaling is a potential SHARPIN target. SHARPIN depletion significantly decreases ERα protein level, ERα target genes expression and estrogen response element activity in breast cancer cells, while SHARPIN overexpression could reverse these effects. SHARPIN depletion significantly decreases estrogen stimulated cell proliferation in breast cancer cells, which effect could be further rescued by ERα overexpression. Further mechanistic study reveals that SHARPIN mainly localizes in the cytosol and interacts with ERα both in the cytosol and the nuclear. SHARPIN regulates ERα signaling through protein stability, not through gene expression. SHARPIN stabilizes ERα protein via prohibiting ERα protein poly-ubiquitination. Further study shows that SHARPIN could facilitate the mono-ubiquitinaiton of ERα at K302/303 sites and facilitate ERE luciferase activity. Together, our findings propose a novel ERα modulation mechanism in supporting breast cancer cell growth, in which SHARPIN could be one suitable target for development of novel therapy for ERα positive breast cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.