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      OTUD6B-AS1 Inhibits Viability, Migration, and Invasion of Thyroid Carcinoma by Targeting miR-183-5p and miR-21

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          Abstract

          Background: The long noncoding RNA (lncRNA) functions as a regulator of initiation, progression, and metastasis of thyroid carcinomas. lncRNA OTUD6B antisense RNA 1 (OTUD6B-AS1) is a tumor-suppressive noncoding RNA in clear cell renal cell carcinoma. The role of OTUD6B-AS1 in thyroid carcinomas has not been reported yet. We aim to investigate the expression and biological functions of OTUD6B-AS1 in thyroid carcinomas.

          Methods: The expression level of OTUD6B-AS1 was measured in 60 paired human thyroid carcinoma tissues and corresponding adjacent normal thyroid tissues. The correlations between the OTUD6B-AS1 expression levels and clinicopathological features were evaluated using the Mann-Whitney test. The effects of OTUD6B-AS1 on thyroid carcinoma cells were determined via the MTT and transwell assays. The potential targets of OTUD6B-AS1 were screened using the online programs OncomiR and StarBase 3.0, and the LncBase Predicted v.2. Luciferase reporter assay was used to confirm the interactions between OTUD6B-AS1 and its potential targets.

          Results: OTUD6B-AS1 was downregulated in thyroid carcinoma tissue samples. The expression of OTUD6B-AS1 correlated with tumor size, clinical stage, and lymphatic metastasis of thyroid carcinoma. Overexpression of OTUD6B-AS1 significantly decreased the viability, migration, and invasion of thyroid carcinoma cells. Online programs predicted miR-183-5p and miR-21 as potential targets of OTUD6B-AS1. Luciferase reporter assays showed miR-183-5p and miR-21 bound to OTUD6B-AS1. Moreover, overexpression of miR-183-5p and miR-21 compromised the inhibitory effects of OTUD6B-AS1 on viability, migration, and invasion of thyroid carcinoma cells.

          Conclusions: Taken together, our findings present in vitro evidence of lncRNA OTUD6B-AS1 as a tumor suppressor in thyroid carcinomas. OTUD6B-AS1 inhibits viability, migration, and invasion of thyroid carcinoma by targeting miR-183-5p and miR-21.

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          LncRNA XIST/miR-34a axis modulates the cell proliferation and tumor growth of thyroid cancer through MET-PI3K-AKT signaling

          Hua Liu, Haoyu Deng, Yajie Zhao … (2018)
          Background Thyroid cancer is one of the most prevalent malignancies in endocrine system. Further understanding and revealing the molecular mechanism underlying thyroid cancer are indispensable for the development of effective diagnosis and treatments. In the present study, we attempted to provide novel basis for targeted therapy for thyroid cancer from the aspect of lncRNA-miRNA-mRNA interaction. Methods The expression and cellular function of XIST (X-inactive specific transcript) was determined. miRNAs which may be direct targets of XIST were screened for from online GEO database and miR-34a was selected. Next, the predicted binding between XIST and miR-34a, and the dynamic effect of XIST and miR-34a on downstream MET (hepatocyte growth factor receptor)-PI3K (phosphoinositide 3-kinase)-AKT (α-serine/threonine-protein kinase) signaling was evaluated. Results XIST was significantly up-regulated in thyroid cancer tissues and cell lines; XIST knockdown suppressed the cell proliferation in vivo and the tumor growth in vitro. Based on online database and online tool prediction results, miR-34a was underexpressed in thyroid cancer and might be a direct target of XIST. Herein, we confirmed the negative interaction between XIST and miR-34a; moreover, XIST knockdown could reduce the protein levels of MET, a downstream target of miR-34a, and the phosphorylation of PI3K and AKT. In thyroid cancer tissues, MET mRNA and protein levels of MET were up-regulated; MET was positively correlated with XIST while negatively correlated with miR-34a, further confirming that XIST serves as a ceRNA for miR-34a through sponging miR-34a, competing with MET for miR-34a binding, and finally modulating thyroid cancer cell proliferation and tumor growth. Conclusion In the present study, we provided novel experimental basis for targeted therapy for thyroid cancer from the aspect of lncRNA-miRNA-mRNA interaction. Electronic supplementary material The online version of this article (10.1186/s13046-018-0950-9) contains supplementary material, which is available to authorized users.
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            Emerging roles of lncRNAs in the post-transcriptional regulation in cancer

            Rong-Zhang He, Di-Xian Luo, Yin-Yuan Mo (2019)
            Accumulating evidence indicates that long non-coding RNAs (lncRNAs) can play a pivotal role in regulation of diverse cellular processes. In particular, lncRNAs can serve as master gene regulators at transcriptional and posttranscriptional levels, leading to tumorigenesis. In this review, we discuss latest developments in lncRNA-meditated gene expression at the post-transcriptional level, including gene splicing, mRNA stability, protein stability and nuclear trafficking.
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              OncomiR: an online resource for exploring pan-cancer microRNA dysregulation

              Alfonso Valencia, Xiaowei Wang, Shuai Chen … (2018)
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Endocrinol (Lausanne)
                Journal ID (iso-abbrev): Front Endocrinol (Lausanne)
                Journal ID (publisher-id): Front. Endocrinol.
                Title: Frontiers in Endocrinology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-2392
                Publication date (Electronic): 17 March 2020
                Publication date Collection: 2020
                Volume: 11
                Electronic Location Identifier: 136
                Affiliations
                Department of General Surgery, Xiangya Hospital, Central South University , Changsha, China
                Author notes

                Edited by: Chun Peng, York University, Canada

                Reviewed by: Guoxiong Xu, Fudan University, China; Nurul-Syakima Ab Mutalib, National University of Malaysia, Malaysia

                *Correspondence: Xinying Li lixinyingchn@ 123456126.com

                This article was submitted to Translational Endocrinology, a section of the journal Frontiers in Endocrinology

                Article
                DOI: 10.3389/fendo.2020.00136
                PMC ID: 7089936
                SO-VID: 30f4313c-fd1f-4937-ae88-9e1d957828b6
                Copyright © Copyright © 2020 Wang, Xia, Feng, Jiang, Wang and Li.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 07 November 2019
                Date accepted : 27 February 2020
                Page count
                Figures: 7, Tables: 3, Equations: 0, References: 45, Pages: 11, Words: 5763
                Funding
                Funded by: Natural Science Foundation of Hunan Province 10.13039/501100004735
                Award ID: No.2019JJ40475
                Categories
                Subject: Endocrinology
                Subject: Original Research

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: lncrna,otud6b-as1,microrna,thyroid carcinoma,mir-183-5p,mir-21
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: lncrna, otud6b-as1, microrna, thyroid carcinoma, mir-183-5p, mir-21

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