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Article type: Other
Authors: Petrovic, Nina* | Davidovic, Radoslav | Bajic, Vladan | Obradovic, Milan | Isenovic, R. Esma
Affiliations: Laboratory of Radiobiology and Molecular Genetics, University of Belgrade-Vinca Institute of Nuclear Sciences, 11000 Belgrade, Serbia
Correspondence: [*] Corresponding author: Nina Petrovic, Laboratory of Radiobiology and Molecular Genetics, University of Belgrade-Vinca Institute of Nuclear Sciences, Mike Petrovica Alasa 12-14, P.O. Box 522, 11000 Belgrade, Serbia. Tel.: +381 11 3408 402; Fax: +381 11 644 74 85; E-mail:dragoninspiration@yahoo.com
Abstract: Breast cancer (BC) is a heterogeneous disease in an urgent need for developing novel research, classification, and therapy approaches. Breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) proteins are well described tumor suppressors with great potential to be the subjects of different therapies. MicroRNAs (miRNAs) are genetic elements that might be used to solve the complex BC puzzle. BRCA1 was described to be the target of up to 100 miRNAs. BRCA1 may directly repress miR-155 activity. In addition, miR-15/107/182-mediated downregulation of BRCA1 interrupt DNA repair and may change the course of BC therapy. miR-146a and miR-146-5p silencing BRCA1 may trigger formation of triple-negative and basal-like sporadic BC cases. miR-182 might effect the therapy outcome. miR-21 targeted therapy might be useful for the treatment of BRCA2 mutation carriers. miR-342 overexpression and the absence of functional BRCA1 gene might cause synthetic lethality, which might be used as a base for future therapies. The present review discusses the latest data from studies that focus on the complex network of miRNAs and BRCA1/2 related BCs, which might be important for improving the therapy within the patients with triple-negative BC (TNBC) and basal-like BC, and for understanding the formation of TNBC.
Keywords: Breast cancer, miRNA, BRCA1, BRCA2, TNBC
DOI: 10.3233/CBM-160319
Journal: Cancer Biomarkers, vol. 19, no. 2, pp. 119-128, 2017
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