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      CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13

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          Abstract

          The circular RNA ciRS-7 has been reported to be involved in the pathogenesis of various tumors, including gastric and colorectal cancer. However, the role of ciRS-7 in esophageal squamous cell carcinoma (ESCC) remains unsolved. In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival. Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell proliferation, migration and invasion in vitro as well as tumor growth and lung metastasis in vivo. Mechanistically, ciRS-7 functioned as the sponge of miR-7 and reactivated its downstream HOXB13-mediated NF-κB/p65 pathway. Conclusively, our findings demonstrate how ciRS-7 induces malignant progression of ESCC and that ciRS-7 may act as a novel prognostic marker and therapeutic target for this lethal disease.

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          Modulating Hox gene functions during animal body patterning.

          Joseph Pearson, Derek Lemons, William McGinnis (2005)
          With their power to shape animal morphology, few genes have captured the imagination of biologists as the evolutionarily conserved members of the Hox clusters have done. Recent research has provided new insight into how Hox proteins cause morphological diversity at the organismal and evolutionary levels. Furthermore, an expanding collection of sequences that are directly regulated by Hox proteins provides information on the specificity of target-gene activation, which might allow the successful prediction of novel Hox-response genes. Finally, the recent discovery of microRNA genes within the Hox gene clusters indicates yet another level of control by Hox genes in development and evolution.
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            The circular RNA Cdr1as, via miR-7 and its targets, regulates insulin transcription and secretion in islet cells

            Huanyu Xu, Sen Guo, Wei Li … (2015)
            Among the identified thousands of circular RNAs (circRNA) in humans and animals, Cdr1as (also known as CiRS-7) was recently demonstrated to act as a powerful miR-7 sponge/inhibitor in developing midbrain of zebrafish, suggesting a novel mechanism for regulating microRNA functions. MiR-7 is abundantly expressed in islet cells, but overexpressing miR-7 in transgenic mouse β cells causes diabetes. Therefore, we infer that Cdr1as expression may inhibit miR-7 function in islet cells, which in turn improves insulin secretion. Here, we show the first characterization of Cdr1as expression in islet cells, which was upregulated by long-term forskolin and PMA stimulation, but not high glucose, indicating the involvement of cAMP and PKC pathways. Remarkably, both insulin content and secretion were significantly increased by overexpression of Cdr1as in islet cells. We further identified a new target Myrip in the Cdr1as/miR-7 pathway that regulates insulin granule secretion, and also another target Pax6 that enhances insulin transcription. Taken together, our findings revealed the effects of the strongly interacting pair of Cdr1as/miR-7 on insulin secretion, which may become a new target for improving β cell function in diabetes.
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              microRNA-7 inhibits the epidermal growth factor receptor and the Akt pathway and is down-regulated in glioblastoma.

              Benjamin Kefas, Jakub Godlewski, Laurey Comeau … (2008)
              microRNAs are noncoding RNAs inhibiting expression of numerous target genes, and a few have been shown to act as oncogenes or tumor suppressors. We show that microRNA-7 (miR-7) is a potential tumor suppressor in glioblastoma targeting critical cancer pathways. miR-7 potently suppressed epidermal growth factor receptor expression, and furthermore it independently inhibited the Akt pathway via targeting upstream regulators. miR-7 expression was down-regulated in glioblastoma versus surrounding brain, with a mechanism involving impaired processing. Importantly, transfection with miR-7 decreased viability and invasiveness of primary glioblastoma lines. This study establishes miR-7 as a regulator of major cancer pathways and suggests that it has therapeutic potential for glioblastoma.
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                Author and article information

                Contributors
                Ming-hao Fang: 86-158-7143-1260 , fangmh@tjh.tjmu.edu.cn
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 6 August 2018
                Publication date PMC-release: 6 August 2018
                Publication date Collection: August 2018
                Volume: 9
                Issue: 8
                Electronic Location Identifier: 838
                Affiliations
                [1 ]ISNI 0000 0004 0368 7223, GRID grid.33199.31, Department of General Medicine, Tongji Medical College, , Huazhong University of Science & Technology, ; Wuhan, 430030 China
                [2 ]ISNI 0000 0004 0368 7223, GRID grid.33199.31, Department of Emergency Medicine, Tongji Medical College, , Huazhong University of Science & Technology, ; Wuhan, 430030 China
                [3 ]ISNI 0000 0004 0368 7223, GRID grid.33199.31, Department of hematology, Tongji Medical College, , Huazhong University of Science & Technology, ; Wuhan, 430030 China
                [4 ]Department of Cardiovascular Medicine, Ezhou Central Hospital of Hubei, Ezhou, 436000 China
                Article
                Publisher ID: 852
                DOI: 10.1038/s41419-018-0852-y
                PMC ID: 6079012
                PubMed ID: 30082829
                SO-VID: 8eb0fc25-112d-43ee-a702-851ba315f2a3
                Copyright © © The Author(s) 2018
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 22 April 2018
                Date revision received : 29 May 2018
                Date accepted : 15 June 2018
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Cell biology
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                ScienceOpen disciplines: Cell biology

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