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      Detection and analysis of circulating large intergenic non‐coding RNA regulator of reprogramming in plasma for breast cancer

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          Abstract

          Background

          Previous studies have indicated that large intergenic non‐coding RNA regulator of reprogramming (lincRNA‐ROR) plays an important role in regulating tumor carcinogenesis and metastasis; however, whether circulating lincRNA‐ROR could function as a potential biomarker for breast cancer (BC) diagnosis and monitoring is unknown. This study was conducted to investigate circulating lincRNA‐ROR in plasma as a potential biomarker for BC diagnosis and monitoring.

          Methods

          We performed reverse transcription‐quantitative‐PCR to examine lincRNA‐ROR expression levels in cell lines, 24 pairs of BC tissue samples, and 94 plasma samples from BC patients. Potential correlations between plasma lincRNA‐ROR levels and clinicopathological characteristics were analyzed. A receiver operating characteristic curve was calculated to evaluate the diagnostic values for BC. Pearson correlation analysis of lincRNA‐ROR in plasma samples and the corresponding tissues of the same patients was performed to explore tumor monitoring values.

          Results

          LincRNA‐ROR expression was significantly increased in BC cell lines, tissues, and plasma (all P < 0.01). Plasma lincRNA‐ROR levels were associated with estrogen receptors ( P = 0.042) and lymph node metastasis ( P = 0.046). The area under the receiver operating characteristic curve of plasma lincRNA‐ROR was 0.844 (sensitivity 80.0%, specificity 56.7%), which was higher than carcinoembryonic and carbohydrate antigen 15‐3 values. Moreover, plasma lincRNA‐ROR levels were decreased in postoperative compared to preoperative samples ( P < 0.0001). Plasma lincRNA‐ROR levels moderately correlated with the corresponding tissue level in the same patients (r 2 = 0.638, P < 0.0001).

          Conclusion

          Plasma lincRNA‐ROR may be a potential biomarker for BC diagnosis and a dynamic monitor.

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          Most cited references33

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          Large intergenic non-coding RNA-RoR modulates reprogramming of human induced pluripotent stem cells.

          The conversion of lineage-committed cells to induced pluripotent stem cells (iPSCs) by reprogramming is accompanied by a global remodeling of the epigenome, resulting in altered patterns of gene expression. Here we characterize the transcriptional reorganization of large intergenic non-coding RNAs (lincRNAs) that occurs upon derivation of human iPSCs and identify numerous lincRNAs whose expression is linked to pluripotency. Among these, we defined ten lincRNAs whose expression was elevated in iPSCs compared with embryonic stem cells, suggesting that their activation may promote the emergence of iPSCs. Supporting this, our results indicate that these lincRNAs are direct targets of key pluripotency transcription factors. Using loss-of-function and gain-of-function approaches, we found that one such lincRNA (lincRNA-RoR) modulates reprogramming, thus providing a first demonstration for critical functions of lincRNAs in the derivation of pluripotent stem cells.
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            Endogenous miRNA sponge lincRNA-RoR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal.

            The embryonic stem cell (ESC) transcriptional and epigenetic networks are controlled by a multilayer regulatory circuitry, including core transcription factors (TFs), posttranscriptional modifier microRNAs (miRNAs), and some other regulators. However, the role of large intergenic noncoding RNAs (lincRNAs) in this regulatory circuitry and their underlying mechanism remains undefined. Here, we demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. We show that linc-RoR shares miRNA-response elements with these core TFs and that linc-RoR prevents these core TFs from miRNA-mediated suppression in self-renewing human ESC. We suggest that linc-RoR forms a feedback loop with core TFs and miRNAs to regulate ESC maintenance and differentiation. These results may provide insights into the functional interactions of the components of genetic networks during development and may lead to new therapies for many diseases. Copyright © 2013 Elsevier Inc. All rights reserved.
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              MicroRNAs: New Biomarkers for Diagnosis, Prognosis, Therapy Prediction and Therapeutic Tools for Breast Cancer

              Dysregulation of microRNAs (miRNAs) is involved in the initiation and progression of several human cancers, including breast cancer (BC), as strong evidence has been found that miRNAs can act as oncogenes or tumor suppressor genes. This review presents the state of the art on the role of miRNAs in the diagnosis, prognosis, and therapy of BC. Based on the results obtained in the last decade, some miRNAs are emerging as biomarkers of BC for diagnosis (i.e., miR-9, miR-10b, and miR-17-5p), prognosis (i.e., miR-148a and miR-335), and prediction of therapeutic outcomes (i.e., miR-30c, miR-187, and miR-339-5p) and have important roles in the control of BC hallmark functions such as invasion, metastasis, proliferation, resting death, apoptosis, and genomic instability. Other miRNAs are of interest as new, easily accessible, affordable, non-invasive tools for the personalized management of patients with BC because they are circulating in body fluids (e.g., miR-155 and miR-210). In particular, circulating multiple miRNA profiles are showing better diagnostic and prognostic performance as well as better sensitivity than individual miRNAs in BC. New miRNA-based drugs are also promising therapy for BC (e.g., miR-9, miR-21, miR34a, miR145, and miR150), and other miRNAs are showing a fundamental role in modulation of the response to other non-miRNA treatments, being able to increase their efficacy (e.g., miR-21, miR34a, miR195, miR200c, and miR203 in combination with chemotherapy).
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                Author and article information

                Contributors
                13308216138@163.com
                liujb7203@163.com
                Journal
                Thorac Cancer
                Thorac Cancer
                10.1111/(ISSN)1759-7714
                TCA
                Thoracic Cancer
                John Wiley & Sons Australia, Ltd (Melbourne )
                1759-7706
                1759-7714
                01 November 2017
                January 2018
                : 9
                : 1 ( doiID: 10.1111/tca.2018.9.issue-1 )
                : 66-74
                Affiliations
                [ 1 ] Department of Laboratory Medicine The Affiliated Hospital of Southwest Medical University Luzhou China
                [ 2 ] Department of Laboratory Medicine West China Hospital, Sichuan University Chengdu China
                [ 3 ] Department of Laboratory Medicine Sichuan Cancer Hospital Chengdu China
                Author notes
                [*] [* ] Correspondence

                Jinbo Liu, Department of Laboratory Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.

                Tel: +86 83 0316 5730

                Fax: +86 83 0316 5730

                Email: liujb7203@ 123456163.com

                Li Zhang, Department of Laboratory Medicine, Sichuan Cancer Hospital, Chengdu, Sichuan 610041, China.

                Tel: +86 28 8542 2344

                Fax: +86 28 8542 2344

                Email: 13308216138@ 123456163.com

                [†]

                These authors contributed equally to this work.

                Author information
                http://orcid.org/0000-0002-5459-0144
                Article
                TCA12537
                10.1111/1759-7714.12537
                5754303
                29090518
                d394e60c-6f7d-4ff2-926e-5e0094f5f1ba
                © 2017 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd

                This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 11 August 2017
                : 12 September 2017
                : 12 September 2017
                Page count
                Figures: 4, Tables: 3, Pages: 9, Words: 5952
                Funding
                Funded by: The Science & Technology Department of Sichuan Province
                Award ID: 14JC0801
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                tca12537
                January 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:5.2.8 mode:remove_FC converted:04.01.2018

                breast cancer,lincrna‐ror,plasma biomarker
                breast cancer, lincrna‐ror, plasma biomarker

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