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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      lncRNA HAND2-AS1 Regulates Prostate Cancer Cell Growth Through Targeting the miR-106a-5p/RBM24 Axis

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          Abstract

          Introduction

          Increasing evidence has shown that abnormally expressed long non-coding RNA (lncRNA) plays crucial roles in prostate cancer (PCa) progression.

          Materials and Methods

          Here, we analyzed the expression level of lncRNA HAND2 antisense RNA 1 (HAND2-AS1) in PCa cells and tissues. Function assays were performed to investigate the biological roles of HAND2-AS1 in PCa cell behaviors. Bioinformatics methods, luciferase activity reporter assay, and RNA pull-down assay were performed to validate the connection of microRNA-106a-5p (miR-106a-5p) with HAND2-AS1. Also, the target of miR-106a-5p was explored using the same methods.

          Results

          Our results revealed HAND2-AS1 expression was decreased in both PCa cells and tissues. In vitro functional assays showed HAND2-AS1 could inhibit PCa cell proliferation and colony formation through promoting cell apoptosis. Dual-luciferase activity assays showed miR-106a-5p could directly bind with HAND2-AS1 and RNA binding motif protein 24 (RBM24). Mechanistically, we showed that HAND2-AS1 regulates PCa cell behaviors via targeting miR-106a-5p/RBM24 axis.

          Conclusion

          In summary, our results illustrated that HAND2-AS1 functions as miR-106a-5p sponge to regulate RBM24 expression, and to influence PCa progression.

          Most cited references13

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          The Diagnosis and Treatment of Prostate Cancer: A Review.

          Prostate cancer is the most common cancer diagnosis made in men with more than 160 000 new cases each year in the United States. Although it often has an indolent course, prostate cancer remains the third-leading cause of cancer death in men.
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            LncRNA NEAT1 promotes docetaxel resistance in prostate cancer by regulating ACSL4 via sponging miR-34a-5p and miR-204-5p

            Docetaxel resistance remains one of the main problems in clinical treatment of metastatic prostate cancer (PCa). Previous studies identified differently expressed lncRNAs in docetaxel-resistant PCa cell lines, while the potential mechanisms were still unknown. In the present study, we found NEAT1 was expressed at high levels in docetaxel-resistant PCa clinical samples and related cell lines. When knockdown NEAT1, cell proliferation and invasion in docetaxel-resistant PCa cells in vitro and in vivo were downregulated. Our further researches explained that NEAT1 exerts oncogenic function in PCa by competitively 'sponging' both miR-34a-5p and miR-204-5p. Inhibition of miR-34a-5p or miR-204-5p expression mimics the docetaxel-resistant activity of NEAT1, whereas ectopic expression of miR-34a-5p or miR-204-5p attenuates the anti-drug function of NEAT1 in PCa cells. Besides, we also found ACSL4 is a target of both miR-34a-5p and miR-204-5p, and ACSL4 was also inhibited by miR-34a-5p and miR-204-5p. Moreover, suppression of miR-34a-5p or/and miR-204-5p greatly restrained the expression of ACSL4 upon NEAT1 overexpression. Joint expression of miR-34a-5p and miR-204a-5p synergistically decreased the expression of ASCL4, indicating miR-34a-5p and miR-204a-5p collaboratively inhibit the expression of ACSL4. Innovatively, we concluded that NEAT1 contributes to the docetaxel resistance by increasing ACSL4 via sponging miR-34a-5p and miR-204-5p in PCa cells.
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              RBM24 suppresses cancer progression by upregulating miR-25 to target MALAT1 in nasopharyngeal carcinoma

              Abnormal interaction between non-coding RNAs has been demonstrated to be a common molecular event in various human cancers, but its significance and underlying mechanisms have not been well documented. RNA-binding proteins (RBPs) are key regulators of RNA transcription and post-transcriptional processing. In this study, we found that RNA-binding protein 24 (RBM24) was frequently downregulated in nasopharyngeal carcinoma (NPC). The restoration of RBM24 expression suppressed NPC cellular proliferation, migration and invasion and impeded metastatic colonization in mouse models. Microarray analyses revealed that miR-25 expression was upregulated by RBM24 expression in NPC cells. Similarly, ectopic miR-25 expression suppressed NPC cellular growth and motility by targeting the pro-oncogenic lncRNA MALAT1, and the knockdown of MALAT1 expression exhibited similar effects as RBM24 restoration in NPC cells. Overall, these findings suggest a novel role of RBM24 as a tumor suppressor. Mechanistically, RBM24 acts at least in part through upregulating the expression of miR-25, which in turn targets MALAT1 for degradation.
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                Author and article information

                Journal
                Onco Targets Ther
                Onco Targets Ther
                OTT
                ott
                OncoTargets and therapy
                Dove
                1178-6930
                21 May 2020
                2020
                : 13
                : 4523-4531
                Affiliations
                [1 ]Department of Urology, Luoyang Central Hospital Affiliated to Zhengzhou University , Luoyang 471000, People’s Republic of China
                [2 ]Central Sterile Supply Department, Shandong Provincial Hospital Affiliated to Shandong University , Jinan, People’s Republic of China
                [3 ]Urinary Surgery, YiDu Central Hospital in Weifang City , Qingzhou, People’s Republic of China
                [4 ]Department of Gynecology, Shandong Provincial Maternity and Childcare Hospital , Jinan, People’s Republic of China
                [5 ]Department of Urology, Shandong Provincial Hospital Affiliated to Shandong University , Jinan 250014, People’s Republic of China
                [6 ]Department of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University , Jinan 250014, People’s Republic of China
                Author notes
                Correspondence: Lianjun Li Department of Urology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250014, P. R. China , Department of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University , Jinan250014, People’s Republic of China Email lilianjun_jn@126.com
                Article
                246274
                10.2147/OTT.S246274
                7247600
                32547083
                1660c79d-de3a-4639-974c-582e8b8df745
                © 2020 Wei et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 16 January 2020
                : 07 April 2020
                Page count
                Figures: 5, References: 17, Pages: 9
                Categories
                Original Research

                Oncology & Radiotherapy
                hand2-as1,mir-106a-5p,rbm24,prostate cancer
                Oncology & Radiotherapy
                hand2-as1, mir-106a-5p, rbm24, prostate cancer

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