Abstract
The regulatory and functional roles of non-coding RNAs are increasingly demonstrated as critical in cancer. Among non-coding RNAs, microRNAs (miRNAs) are the most well-studied with direct regulation of biological signals through post-transcriptional repression of mRNAs. Like the transcriptome, which varies between tissue type and disease condition, the miRNA landscape is also similarly altered and shows disease-specific changes. The importance of individual tumor-promoting or suppressing miRNAs is well documented in breast cancer; however, the implications of miRNA networks is less defined. Some evidence suggests that breast cancer subtype-specific cellular effects are influenced by distinct miRNAs and a comprehensive network of subtype-specific miRNAs and mRNAs would allow us to better understand breast cancer signaling. In this review, we discuss the altered miRNA landscape in the context of breast cancer and propose that breast cancer subtypes have distinct miRNA dysregulation. Further, given that miRNAs can be used as diagnostic and/or prognostic biomarkers, their impact as novel targets for subtype-specific therapy is also possible and suggest important implications for subtype-specific miRNAs.
Highlights
The seminal paper was the first to suggest the regulation of a protein (LIN14) through complementary sequence interaction of the miRNA with the 30 untranslated region (UTR) of the lin-14 mRNA
Case control study of estrogen receptor/progesterone receptor positive (ER/PR +) patients with tamoxifen treatment miR-221 expression is high in ER/PR + patients and is not changed by KI67/PR levels miR-221
In early-stage breast cancer, miR-135b-5p repression resulted in migration through the syndecan-binding protein (SDCBP) [85]. These findings strongly suggest that miR-135-5p has a role in the regulation of migration processes in breast cancer, with functional difference among different subtypes arising from context-specific signaling networks
Summary
The first microRNA (miRNA), lin-4, was identified in Caenorhabditis elegans [1]. Dicer recognizes the single nucleotide overhangs of the stem loop pri-miRNA, and the Dicer–RNA complex is stabilized by the trans-activation-responsive RNA binding protein (TARBP2) [3,10] This duplex RNA is bound by Argonaute protein AGO to form RNA induced silencing complex (RISC) and generate the mature miRNAs [11]. One of the mature miRNA strands (passenger strand) is degraded by the nuclease activity of AGO2, while the other strand (guide strand) is incorporated into RISC, and subsequently regulates post-transcriptional gene expression via binding to complementary sequences in mRNA targets. This typically results in the downregulation of target mRNAs by inhibiting their translation and/or mediating their degradation via RISC [4,5,7–9]. In breast cancer the importance of miRNAs is evident in the progression of the disease, and in the specific breast subtypes which define the disease clinically and molecularly and is the focus of this review
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
