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      A circular twist on microRNA regulation

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      Author(s): 1 , 1 , 1 , *
      Publication date (Electronic):
      Journal: Cell Research
      Publisher: Nature Publishing Group

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          Abstract

          Circular RNAs (circRNAs) are a novel class of RNA whose physiological function has yet to be investigated. A recent publication in Science provides the first evidence of the biological relevance of a circRNA in an in vivo model and unveils an unexpected twist on their crosstalk with miRNAs.

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          Oncogenic Role of Fusion-circRNAs Derived from Cancer-Associated Chromosomal Translocations.

          Jlenia Guarnerio, Marco Bezzi, Jong Jeong … (2016)
          Chromosomal translocations encode oncogenic fusion proteins that have been proven to be causally involved in tumorigenesis. Our understanding of whether such genomic alterations also affect non-coding RNAs is limited, and their impact on circular RNAs (circRNAs) has not been explored. Here, we show that well-established cancer-associated chromosomal translocations give rise to fusion circRNAs (f-circRNA) that are produced from transcribed exons of distinct genes affected by the translocations. F-circRNAs contribute to cellular transformation, promote cell viability and resistance upon therapy, and have tumor-promoting properties in in vivo models. Our work expands the current knowledge regarding molecular mechanisms involved in cancer onset and progression, with potential diagnostic and therapeutic implications.
          Article 0 comments Cited 316 times – based on 0 reviews     Review now
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            Circular transcripts of the testis-determining gene Sry in adult mouse testis

            Blanche Capel, Amanda Swain, Silvia K. Nicolis … (1993)
            Article 0 comments Cited 139 times – based on 0 reviews     Review now
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              Is Open Access

              Silencing CDR1as inhibits colorectal cancer progression through regulating microRNA-7

              Wentao Tang, Meiling Ji, Guodong He … (2017)
              An increasing number of studies have demonstrated that circular RNAs (circRNAs) can regulate gene expression through interacting with microRNAs. In this study, we analyzed the expression of antisense to CDR1as in colorectal cancer (CRC). CDR1as had a higher expression in CRC tissues compared to adjacent, normal mucosa and was positively associated with tumor size, T stage, lymph node metastasis, and poor overall survival (OS). Downregulation of CDR1as suppressed CRC cell proliferation and invasion and increased microRNA-7 (miR-7) expression. Intriguingly, ectopic expression of miR-7 in CRC cells consistently inhibited proliferation and invasion, and the miR-7 inhibitor was able to rescue the function of CDR1as knockdown. Mechanistic studies demonstrated that CDR1as silencing suppressed EGFR and IGF-1R expression, which could be partially blocked by the miR-7 inhibitor. Finally, positive correlations between CDR1as expression and EGFR and IGF-1R expression were observed in CRC samples. Thus, given the importance of CDR1as in blocking miR-7 and positively regulating EGFR and IGF-1R, dysregulated CDR1as expression may play an important role in CRC progression.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cell Res
                Journal ID (iso-abbrev): Cell Res
                Title: Cell Research
                Publisher: Nature Publishing Group
                ISSN (Print): 1001-0602
                ISSN (Electronic): 1748-7838
                Publication date (Print): December 2017
                Publication date (Electronic): 31 October 2017
                Volume: 27
                Issue: 12
                Pages: 1401-1402
                Affiliations
                [1 ] Cancer Research Institute, Beth Israel Deaconess Cancer Center, Department of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School , Boston, MA 02215, USA
                Author notes
                Article
                Accession ID: PMC5717405 Pmcid ID: PMC5717405 Pmc-uid ID: 5717405 Publisher Item ID: cr2017136
                DOI: 10.1038/cr.2017.136
                PMC ID: 5717405
                PubMed ID: 29086764
                SO-VID: d8671fd7-8b68-4390-bc71-6c764394fb38
                Copyright © Copyright © 2017 Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
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                Subject: Research Highlight

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