ArticleFrontiers in genetics2016
Post-transcriptional Regulation of BRCA2 through Interactions with miR-19a and miR-19b.
Article in Frontiers in genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 27 citations in OpenAlex.
- An integrated analysis of microRNAs regulating DNA damage response in triple-negative breast cancer.Breast cancer (Tokyo, Japan) · 2023Article
- The Breast Cancer Protooncogenes HER2, BRCA1 and BRCA2 and Their Regulation by the iNOS/NOS2 Axis.Antioxidants (Basel, Switzerland) · 2022Review
- Investigation of BRCAness associated miRNA-gene axes in breast cancer: cell-free miR-182-5p as a potential expression signature of BRCAness.BMC cancer · 2022Article
- Whole transcriptome analysis of RNA expression profiles reveals the potential regulating action of long noncoding RNA in lactating cows fed a high concentrate diet.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2021Article
- Proteogenomic Workflow Reveals Molecular Phenotypes Related to Breast Cancer Mammographic Appearance.Journal of proteome research · 2021Article
- Jack of all trades? The versatility of RNA in DNA double-strand break repair.Essays in biochemistry · 2020Review
- Regulation of breast cancer metastasis signaling by miRNAs.Cancer metastasis reviews · 2020Review
- Radiosensitization of Hepatocellular Carcinoma through Targeting Radio-Associated MicroRNA.International journal of molecular sciences · 2020Review
- lncRNA-SNHG14 Promotes Atherosclerosis by Regulating RORComputational and mathematical methods in medicine · 2020Article
- miR-19b-3p promotes human pancreatic cancer Capan-2 cells proliferation by targeting phosphatase and tension homolog.Annals of translational medicine · 2019Article
- Review
- Non-Coding Variants inCancers · 2018Review
- Regulation of DNA Double-Strand Break Repair by Non-Coding RNAs.Molecules (Basel, Switzerland) · 2018Review
- Oncogenic and Tumor-Suppressive Roles of MicroRNAs with Special Reference to Apoptosis: Molecular Mechanisms and Therapeutic Potential.Molecular diagnosis & therapy · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer type 2, early onset susceptibility gene (BRCA2) is a major component of the homologous recombination DNA repair pathway. It acts as a tumor suppressor whose function is often lost in cancers. Patients with specific mutations in the BRCA2 gene often display discrete clinical, histopathological, and molecular features. However, a subset of sporadic cancers has wild type BRCA2 and display defects in the homology-directed repair pathway, which is the hallmark of 'BRCAness.' The mechanisms by which BRCAness arises are not well understood but post-transcriptional regulation of BRCA2 gene expression by microRNAs (miRNAs) may contribute to this phenotype. Here, we examine the post-transcriptional effects that some members of the six-miRNA cluster known as the miR-17/92 cluster have on the abundance of BRCA2's messenger RNA (mRNA) and protein. We discuss two interactions involving the miR-19a and miR-19b members of the cluster and the 3'UTR of BRCA2's mRNA. We investigated these miRNA:mRNA interactions in 15 cell lines derived from pancreatic, breast, colon, and kidney tissue. We show that over-expression of these two miRNAs results in a concomitant decrease of BRCA2's mRNA and protein expression in a subset of the tested cell lines. Additionally, using luciferase reporter assays we identified direct interactions between miR-19a/miR-19b and a miRNA response element (MRE) in BRCA2's 3'UTR. Our results suggest that BRCA2 is subject to a complex post-transcriptional regulatory program that has specific dependencies on the genetic and phenotypic background of cell types.
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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.