ArticleNeoplasia (New York, N.Y.)2020
TRIM11 promotes breast cancer cell proliferation by stabilizing estrogen receptor α.
Article in Neoplasia (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- E3 Ubiquitin Ligases in Breast Cancer Metastasis: A Systematic Review of Pathogenic Functions and Clinical Implications.Frontiers in oncology · 2021Pooled it
- TRIM Protein Superfamily in Breast Cancer: Yin and Yang.Biochemical genetics · 2026Review
- Amyloid Precursor Protein Processing Links Female Urgency Urinary Incontinence with Alzheimer's Disease: Implications for Treatment.International journal of molecular sciences · 2026Article
- Nucleic sexual hormone receptor signaling pathways in breast cancer: function regulation, crosstalk, and therapeutic implications.NPJ precision oncology · 2026Review
- The METTL3/IGF2BP1 axis-mediated m6 A modification of TRIM11 mRNA suppresses ferroptosis and accelerates malignant progression in non-small cell lung cancer cells by degrading ACSL4.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- TRIM47 promotes hypopharyngeal and laryngeal cancers progression through promoting K63-linked ubiquitination of vimentin.Cancer science · 2025Article
- A Review of Anticancer Potential of Conferone, Diversin and Ferutinin; Which One is Stronger for Cancer Therapy?Anti-cancer agents in medicinal chemistry · 2025Review
- Decoding estrogen receptor and GPER biology: structural insights and therapeutic advances in ERα-positive breast cancer.Frontiers in oncology · 2025Review
- UBR1 promotes anaplastic thyroid carcinoma progression via stabilizing YAP through monoubiquitylation.Scientific reports · 2024Article
- KDM5 family as therapeutic targets in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Molecular cancer · 2024Review
- USP15 promotes the progression of papillary thyroid cancer by regulating HMGB1 stability through its deubiquitination.Journal of Cancer · 2024Article
- Participation of protein metabolism in cancer progression and its potential targeting for the management of cancer.Amino acids · 2023Review
- Estrogen Receptor Signaling in Breast Cancer.Cancers · 2023Review
- Stabilization of estrogen receptor α by USP37 contributes to the progression of breast cancer.Cancer science · 2023Article
- Cutaneous melanocytic tumor with CRTC1::TRIM11 fusion and prominent epidermal involvement: A case report.Journal of cutaneous pathology · 2022Article
- Targeting UBR5 in hepatocellular carcinoma cells and precise treatment via echinacoside nanodelivery.Cellular & molecular biology letters · 2022Article
- Regulation of KDM5C stability and enhancer reprogramming in breast cancer.Cell death & disease · 2022Article
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- USP26 promotes anaplastic thyroid cancer progression by stabilizing TAZ.Cell death & disease · 2022Article
- The Role of SUMO E3 Ligases in Signaling Pathway of Cancer Cells.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is the most commonly diagnosed malignancy in female worldwide, over 70% of which are estrogen receptor α (ERα) positive. ERα has a crucial role in the initiation and progression of breast cancer and is an indicator of endocrine therapy, while endocrine resistance is an urgent problem in ER-positive breast cancer patients. In the present study, we identify a novel E3 ubiquitin ligase TRIM11 function to facilitate ERα signaling. TRIM11 is overexpressed in human breast cancer, and associates with poor prognosis. The protein level of TRIM11 is highly correlated with ERα. RNA-seq results suggest that ERα signaling may be an underlying target of TRIM11. Depletion of TRIM11 in breast cancer cells significantly decreases cell proliferation and migration. And the suppression effects can be reversed by overexpressing ERα. In addition, ERα protein level, ERα target genes expression and estrogen response element activity are also dramatically decreased by TRIM11 depletion. Further mechanistic analysis indicates that the RING domain of TRIM11 interacted with the N terminal of ERα in the cytoplasm and promotes its mono-ubiquitination, thus enhances ERα protein stability. Our study describes TRIM11 as a modulating factor of ERα and increases ERα stability via mono-ubiquitination. TRIM11 could be a promising therapeutic target for breast cancer treatment.
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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.