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      Systematic characterization of non‐coding RNAs in triple‐negative breast cancer

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          Abstract

          Triple‐negative breast cancer (TNBC) is one of the most aggressive subtypes of breast cancer with negativity for oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor (HER2). Non‐coding RNAs (ncRNAs) make up most of the transcriptome and are widely present in eukaryotic cells. In recent years, emerging evidence suggests that ncRNAs, mainly microRNAs (miRNAs), long ncRNAs (lncRNAs) and circular RNAs (circRNAs), play prominent roles in the tumorigenesis and development of TNBC, but the functions of most ncRNAs have not been fully described. In this review, we systematically elucidate the general characteristics and biogenesis of miRNAs, lncRNAs and circRNAs, discuss the emerging functions of these ncRNAs in TNBC and present future perspectives in clinical practice.

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          Novel Role of FBXW7 Circular RNA in Repressing Glioma Tumorigenesis

          Yibing Yang, Xinya Gao, Maolei Zhang … (2017)
          Abstract Background Circular RNAs (circRNAs) are RNA transcripts that are widespread in the eukaryotic genome. Recent evidence indicates that circRNAs play important roles in tissue development, gene regulation, and carcinogenesis. However, whether circRNAs encode functional proteins remains elusive, although translation of several circRNAs was recently reported. Methods CircRNA deep sequencing was performed by using 10 pathologically diagnosed glioblastoma samples and their paired adjacent normal brain tissues. Northern blotting, Sanger sequencing, antibody, and liquid chromatograph Tandem Mass Spectrometer were used to confirm the existence of circ-FBXW7 and its encoded protein in in two cell lines. Lentivirus-transfected stable U251 and U373 cells were used to assess the biological functions of the novel protein in vitro and in vivo (five mice per group). Clinical implications of circ-FBXW7 were assessed in 38 pathologically diagnosed glioblastoma samples and their paired periphery normal brain tissues by using quantitative polymerase chain reaction (two-sided log-rank test). Results Circ-FBXW7 is abundantly expressed in the normal human brain (reads per kilobase per million mapped reads [RPKM] = 9.31). The spanning junction open reading frame in circ-FBXW7 driven by internal ribosome entry site encodes a novel 21-kDa protein, which we termed FBXW7-185aa. Upregulation of FBXW7-185aa in cancer cells inhibited proliferation and cell cycle acceleration, while knockdown of FBXW7-185aa promoted malignant phenotypes in vitro and in vivo. FBXW7-185aa reduced the half-life of c-Myc by antagonizing USP28-induced c-Myc stabilization. Moreover, circ-FBXW7 and FBXW7-185aa levels were reduced in glioblastoma clinical samples compared with their paired tumor-adjacent tissues (P < .001). Circ-FBXW7 expression positively associated with glioblastoma patient overall survival (P = .03). Conclusions Endogenous circRNA encodes a functional protein in human cells, and circ-FBXW7 and FBXW7-185aa have potential prognostic implications in brain cancer.
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            miRNA-mediated gene silencing by translational repression followed by mRNA deadenylation and decay.

            S. Djuranovic, A. Nahvi, R. Green (2012)
            microRNAs (miRNAs) regulate gene expression through translational repression and/or messenger RNA (mRNA) deadenylation and decay. Because translation, deadenylation, and decay are closely linked processes, it is important to establish their ordering and thus to define the molecular mechanism of silencing. We have investigated the kinetics of these events in miRNA-mediated gene silencing by using a Drosophila S2 cell-based controllable expression system and show that mRNAs with both natural and engineered 3' untranslated regions with miRNA target sites are first subject to translational inhibition, followed by effects on deadenylation and decay. We next used a natural translational elongation stall to show that miRNA-mediated silencing inhibits translation at an early step, potentially translation initiation.
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              Mechanisms of Chemotherapy Resistance in Triple-Negative Breast Cancer—How We Can Rise to the Challenge

              Milica Nedeljković, Ana Damjanović (2019)
              Triple-negative (TNBC) is the most lethal subtype of breast cancer owing to high heterogeneity, aggressive nature, and lack of treatment options. Chemotherapy remains the standard of care for TNBC treatment, but unfortunately, patients frequently develop resistance. Accordingly, in recent years, tremendous effort has been made into elucidating the mechanisms of TNBC chemoresistance with the goal of identifying new molecular targets. It has become evident that the development of TNBC chemoresistance is multifaceted and based on the elaborate interplay of the tumor microenvironment, drug efflux, cancer stem cells, and bulk tumor cells. Alterations of multiple signaling pathways govern these interactions. Moreover, TNBC’s high heterogeneity, highlighted in the existence of several molecular signatures, presents a significant obstacle to successful treatment. In the present, in-depth review, we explore the contribution of key mechanisms to TNBC chemoresistance as well as emerging strategies to overcome them. We discuss novel anti-tumor agents that target the components of these mechanisms and pay special attention to their current clinical development while emphasizing the challenges still ahead of successful TNBC management. The evidence presented in this review outlines the role of crucial pathways in TNBC survival following chemotherapy treatment and highlights the importance of using combinatorial drug strategies and incorporating biomarkers in clinical studies.
              Article 0 comments Cited 289 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yichao Zhu: zhuyichao@njmu.edu.cn
                Chaoying Liu:
                ORCID: https://orcid.org/0000-0003-0484-9522
                liuchaoying666@163.com
                Journal
                Journal ID (nlm-ta): Cell Prolif
                Journal ID (iso-abbrev): Cell Prolif
                Journal ID (doi): 10.1111/(ISSN)1365-2184
                Journal ID (publisher-id): CPR
                Title: Cell Proliferation
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0960-7722
                ISSN (Electronic): 1365-2184
                Publication date (Electronic): 06 April 2020
                Publication date Collection: May 2020
                Volume: 53
                Issue: 5 ( doiID: 10.1111/cpr.v53.5 )
                Electronic Location Identifier: e12801
                Affiliations
                [ 1 ] Department of Oncology Wuxi People's Hospital Affiliated to Nanjing Medical University Wuxi China
                [ 2 ] Department of Physiology Nanjing Medical University Nanjing China
                [ 3 ] State Key Laboratory of Reproductive Medicine Nanjing Medical University Nanjing China
                Author notes
                [*] [* ] Correspondence

                Chaoying Liu, Department of Oncology, Wuxi People's Hospital Affiliated to Nanjing Medical University, 299 Qingyang Road, Wuxi 214023, China.

                Email: liuchaoying666@ 123456163.com

                Yichao Zhu, Department of Physiology, Nanjing Medical University, 101 Longmian Av., Nanjing 211166, China.

                Email: zhuyichao@ 123456njmu.edu.cn

                Author information
                https://orcid.org/0000-0001-7799-8129
                https://orcid.org/0000-0003-0484-9522
                Article
                Publisher ID: CPR12801
                DOI: 10.1111/cpr.12801
                PMC ID: 7260065
                PubMed ID: 32249490
                SO-VID: 879d8b64-6157-404c-a306-0d7ebbb7fd10
                Copyright © © 2020 The Authors. Cell Proliferation Published by John Wiley & Sons Ltd.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 04 February 2020
                Date revision received : 03 March 2020
                Date accepted : 11 March 2020
                Page count
                Figures: 5, Tables: 4, Pages: 19, Words: 13533
                Funding
                Funded by: Foundation of Wuxi Health Commission
                Award ID: QNRC003
                Funded by: Natural Science Foundation of Jiangsu Province of China
                Award ID: BE2017626
                Award ID: BK20181367
                Categories
                Subject: Review
                Subject: Reviews
                Custom metadata
                source-schema-version-number 2.0
                cover-date May 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.3 mode:remove_FC converted:29.05.2020

                ScienceOpen disciplines: Cell biology
                Data availability:
                ScienceOpen disciplines: Cell biology

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