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      Long noncoding RNA MAFG-AS1 facilitates bladder cancer tumorigenesis via regulation of miR-143-3p/SERPINE1 axis

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          Abstract

          Background

          Numerous studies have shown that long noncoding RNAs (lncRNAs) act as key regulators of bladder cancer progression. While lncRNA MAFG-AS1 has been confirmed as an oncogenic molecule in various cancers and tumorigenesis, in present study, we investigated its function and role in the tumorigenesis of bladder cancer.

          Methods

          The expression of MAFG-AS1, miR-143-3p and SERPINE1 in bladder cancer tissues was detected by qRT-PCR methods. The relationship between MAFG-AS1 expression and clinicopathologic characteristics of bladder cancer was analyzed. The effects of MAFG-AS1 depletion on cell proliferation, migration, invasion and apoptosis were investigated. The binding relationship of MAFG-AS1, miR-143-3p and SERPINE1 was examined by luciferase reporter analysis and RNA immunoprecipitation (RIP) assay.

          Results

          MAFG-AS1 was upregulated in bladder cancer tissues and cell lines. High MAFG-AS1 expression was associated with bladder cancer histological grade, TNM stage and lymph node metastasis, and patients with high expression showed poor overall survival. Cell function experiments showed that MAFG-AS1 silencing markedly suppressed bladder cancer cell proliferation, migration, invasion and increased cell apoptosis. Moreover, our results demonstrated that MAFG-AS1 functioned as a competing endogenous RNA for miR-143-3p to modulate SERPINE1 levels. Further analysis showed that miR-143-3p inhibition or SERPINE1 overexpression alleviated the suppressive effects of MAFG-AS1 silencing on malignant features.

          Conclusions

          Our findings indicated that MAFG-AS1 facilitates tumorigenesis via regulation of the miR-143-3p/SERPINE1 axis and also provides a novel insight into tumorigenesis and identify a promising therapeutic target for bladder cancer.

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          Long non-coding RNAs: insights into functions.

          Tim Mercer, Marcel E Dinger, John S. Mattick (2009)
          In mammals and other eukaryotes most of the genome is transcribed in a developmentally regulated manner to produce large numbers of long non-coding RNAs (ncRNAs). Here we review the rapidly advancing field of long ncRNAs, describing their conservation, their organization in the genome and their roles in gene regulation. We also consider the medical implications, and the emerging recognition that any transcript, regardless of coding potential, can have an intrinsic function as an RNA.
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            LNMAT1 promotes lymphatic metastasis of bladder cancer via CCL2 dependent macrophage recruitment

            Changhao Chen, Wang He, Jian Huang … (2018)
            Tumor-associated macrophages (TAMs) are the most abundant inflammatory infiltrates in the tumor microenvironment and contribute to lymph node (LN) metastasis. However, the precise mechanisms of TAMs-induced LN metastasis remain largely unknown. Herein, we identify a long noncoding RNA, termed Lymph Node Metastasis Associated Transcript 1 (LNMAT1), which is upregulated in LN-positive bladder cancer and associated with LN metastasis and prognosis. Through gain and loss of function approaches, we find that LNMAT1 promotes bladder cancer-associated lymphangiogenesis and lymphatic metastasis. Mechanistically, LNMAT1 epigenetically activates CCL2 expression by recruiting hnRNPL to CCL2 promoter, which leads to increased H3K4 tri-methylation that ensures hnRNPL binding and enhances transcription. Furthermore, LNMAT1-induced upregulation of CCL2 recruits macrophages into the tumor, which promotes lymphatic metastasis via VEGF-C excretion. These findings provide a plausible mechanism for LNMAT1-modulated tumor microenvironment in lymphatic metastasis and suggest that LNMAT1 may represent a potential therapeutic target for clinical intervention in LN-metastatic bladder cancer.
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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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                Author and article information

                Journal
                Journal ID (nlm-ta): Transl Cancer Res
                Journal ID (iso-abbrev): Transl Cancer Res
                Journal ID (publisher-id): TCR
                Title: Translational Cancer Research
                Publisher: AME Publishing Company
                ISSN (Print): 2218-676X
                ISSN (Electronic): 2219-6803
                Publication date (Print and electronic): November 2020
                Publication date (Print): November 2020
                Volume: 9
                Issue: 11
                Pages: 7214-7226
                Affiliations
                [1]deptDepartment of Urology, Xiangya Hospital , Central South University , Changsha, China
                Author notes

                Contributions: (I) Conception and design: Y Li; (II) Administrative support: M Mo; (III) Provision of study materials or patients: X Sun, Y Cai; (IV) Collection and assembly of data: X Hu, C Zhao; (V) Data analysis and interpretation: W He; (VI) Manuscript writing: All authors; (VII) Final approval of manuscript: All authors approved the final manuscript.

                Correspondence to: Yangle Li. Department of Urology, Xiangya Hospital, Central South University, No. 87 Xiangya Road, Changsha 410008, China. Email: liyangle2003@ 123456163.com .
                Article
                Publisher ID: tcr-09-11-7214
                DOI: 10.21037/tcr-20-1971
                PMC ID: 8799265
                PubMed ID: 35117325
                SO-VID: 1a8555e6-2246-44d6-8d18-dd49cff0a2b4
                Copyright © 2020 Translational Cancer Research. All rights reserved.
                License:

                Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

                History
                Date received : 01 May 2020
                Date accepted : 20 September 2020
                Funding
                Funded by: the National Youth Science Foundation of China
                Award ID: 81802561
                Categories
                Subject: Original Article

                Keywords: bladder cancer,tumorigenesis,mafg-as1,mir-143-3p,serpine1
                Data availability:
                Keywords: bladder cancer, tumorigenesis, mafg-as1, mir-143-3p, serpine1

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