ArticleNature medicine2011
Tumor suppressor BRCA1 epigenetically controls oncogenic microRNA-155.
Article in Nature medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 134 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
134 citing papers in PubMed, 2 syntheses or guidelines pooled it, 221 citations in OpenAlex.
- Discovery and function exploration of microRNA-155 as a molecular biomarker for early detection of breast cancer.Breast cancer (Tokyo, Japan) · 2021Pooled it
- MicroRNAs as potential signatures of environmental exposure or effect: a systematic review.Environmental health perspectives · 2015Pooled it
- The Landscape of BRCA1-Associated Post-Translational Modifications.Cell biology international · 2026Review
- MicroRNA-Directed Biomarkers and Breast Cancer Therapeutics-Potential to Advance Personalised Approaches in Clinical Trials.International journal of molecular sciences · 2026Review
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- miRNA and Its Implications in the Treatment Resistance in Breast Cancer-Narrative Review of What Do We Know So Far.Non-coding RNA · 2025Review
- Review
- Clinical significance of long non-coding RNA MIR155HG genetic variants and susceptibility to oral cancer.Scientific reports · 2025Article
- The advances in acetylation modification in senescence and aging-related diseases.Frontiers in physiology · 2025Review
- A cross-sectional study comparing the expression of DNA repair molecules in subjects with and without atherosclerotic plaques.Molecular biology reports · 2024Article
- Genomic Alterations Affecting Competitive Endogenous RNAs (ceRNAs) and Regulatory Networks (ceRNETs) with Clinical Implications in Triple-Negative Breast Cancer (TNBC).International journal of molecular sciences · 2024Review
- ALDH1A1 drives prostate cancer metastases and radioresistance by interplay with AR- and RAR-dependent transcription.Theranostics · 2024Article
- miRNA Expression Profiling in Human Breast Cancer Diagnostics and Therapy.Current issues in molecular biology · 2023Review
- In Silico Identification of a BRCA1:miR-29:DNMT3 Axis Involved in the Control of Hormone Receptors in BRCA1-Associated Breast Cancers.International journal of molecular sciences · 2023Article
- MicroRNA-155-5p, Reduced by Curcumin-Re-Expressed HypermethylatedInternational journal of molecular sciences · 2023Article
- Harnessing Epigenetics for Breast Cancer Therapy: The Role of DNA Methylation, Histone Modifications, and MicroRNA.International journal of molecular sciences · 2023Review
- The emergence of Fanconi anaemia type S: a phenotypic spectrum of biallelicFrontiers in oncology · 2023Review
- HDAC2 as a target for developing anti-cancer drugs.Computational and structural biotechnology journal · 2023Review
- The Role of miR-155 in Antitumor Immunity.Cancers · 2022Review
- Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
- Erratum issued
Authors and funding
19 authors at 9 institutions in 3 countries.
Funding
Abstract
BRCA1, a well-known tumor suppressor with multiple interacting partners, is predicted to have diverse biological functions. However, so far its only well-established role is in the repair of damaged DNA and cell cycle regulation. In this regard, the etiopathological study of low-penetrant variants of BRCA1 provides an opportunity to uncover its other physiologically important functions. Using this rationale, we studied the R1699Q variant of BRCA1, a potentially moderate-risk variant, and found that it does not impair DNA damage repair but abrogates the repression of microRNA-155 (miR-155), a bona fide oncomir. Mechanistically, we found that BRCA1 epigenetically represses miR-155 expression via its association with HDAC2, which deacetylates histones H2A and H3 on the miR-155 promoter. We show that overexpression of miR-155 accelerates but the knockdown of miR-155 attenuates the growth of tumor cell lines in vivo. Our findings demonstrate a new mode of tumor suppression by BRCA1 and suggest that miR-155 is a potential therapeutic target for BRCA1-deficient tumors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.