ArticleCancer science2010
Hakai acts as a coregulator of estrogen receptor alpha in breast cancer cells.
Article in Cancer science, 2010. 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, 33 citations in OpenAlex.
- [Construction of a ubiquitination-related gene prognostic model for breast cancer based on taxane treatment response].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Article
- Functional and clinical significance of the RNA mNPJ breast cancer · 2025Article
- Review
- Beyond destruction: emerging roles of the E3 ubiquitin ligase Hakai.Cellular & molecular biology letters · 2025Review
- CBLL1 is hypomethylated and correlates with cortical thickness in transgender men before gender affirming hormone treatment.Scientific reports · 2023Article
- Dynamics and functions of E-cadherin complexes in epithelial cell and tissue morphogenesis.Marine life science & technology · 2023Review
- The emerging role of RNA N6-methyladenosine methylation in breast cancer.Biomarker research · 2021Review
- The role of RNAMolecular therapy. Nucleic acids · 2021Review
- Emerging roles of N6-methyladenosine (mCell & bioscience · 2020Review
- Circ_0072083 interference enhances growth-inhibiting effects of cisplatin in non-small-cell lung cancer cells via miR-545-3p/CBLL1 axis.Cancer cell international · 2020Article
- CBLL1 is highly expressed in non-small cell lung cancer and promotes cell proliferation and invasion.Thoracic cancer · 2019Article
- Ajuba inhibits hepatocellular carcinoma cell growth via targeting of β-catenin and YAP signaling and is regulated by E3 ligase Hakai through neddylation.Journal of experimental & clinical cancer research : CR · 2018Article
- Hakai overexpression effectively induces tumour progression and metastasis in vivo.Scientific reports · 2018Article
- Upregulation of CBLL1 in rat brain cortex after lipopolysaccharide treated.Journal of molecular histology · 2013Article
- Biological influence of Hakai in cancer: a 10-year review.Cancer metastasis reviews · 2012Review
- Structure of a novel phosphotyrosine-binding domain in Hakai that targets E-cadherin.The EMBO journal · 2012Article
- Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Estrogen receptors play a key role in breast cancer development. One of the current therapeutic strategies for the treatment of estrogen receptor (ER)-α-positive breast cancers relies on the blockade of ERα transcriptional activity. In the present study, we characterized Hakai, originally characterized as an E-cadherin binding protein, as a strong blockade of ERα in breast cancer cells. We showed that Hakai inhibited the transcriptional activity of ERα by binding directly to ERα. The DNA-binding domain of ERα was found to be responsible for its interaction with Hakai. Hakai competed with ERα coactivators, such as steroid receptor coactivator-1 (SRC-1) and glucocoriticord receptor interacting protein-1 (GRIP-1), for the modulation of ERα transactivation, while its ubiquitin-ligase activity was not required. Further, overexpression of Hakai inhibited the proliferation and migration of breast cancer cells. Taken together, these results suggest that Hakai is a novel corepressor of ERα and may play a negative role in the development and progression of breast cancers.
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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.