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      Functions and mechanisms of circular RNAs in cancer radiotherapy and chemotherapy resistance

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          Abstract

          Circular RNAs (circRNAs), one type of non-coding RNA, were initially misinterpreted as nonfunctional products of pre-mRNA mis-splicing. Currently, circRNAs have been proven to manipulate the functions of diverse molecules, including non-coding RNAs, mRNAs, DNAs and proteins, to regulate cell activities in physiology and pathology. Accumulating evidence indicates that circRNAs play critical roles in tumor genesis, development, and sensitivity to radiation and chemotherapy. Radiotherapy and chemotherapy are two primary types of intervention for most cancers, but their therapeutic efficacies are usually retarded by intrinsic and acquired resistance. Thus, it is urgent to develop new strategies to improve therapeutic responses. To achieve this, clarification of the underlying mechanisms affecting therapeutic responses in cancer is needed. This review summarizes recent progress and mechanisms of circRNAs in cancer resistance to radiation and chemotherapy, and it discusses the limitations of available knowledge and potential future directions.

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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 313 times – based on 0 reviews     Review now
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            Tumor Cell Biodiversity Drives Microenvironmental Reprogramming in Liver Cancer

            Lichun Ma, Maria O. Hernandez, Yongmei Zhao … (2019)
            Cellular diversity in tumors is key factor for therapeutic failures and lethal outcomes of solid malignancies. Here, we determined the single-cell transcriptomic landscape of liver cancer biospecimens from 19 patients. We found varying degrees of heterogeneity in malignant cells within and between tumors and diverse landscapes of tumor microenvironment (TME). Strikingly, tumors with higher transcriptomic diversity were associated with patient’s worse overall survival. We found a link between hypoxia-dependent VEGF expression in tumor diversity and TME polarization. Moreover, T cells from higher heterogenous tumors showed lower cytolytic activities. Consistent results were found using bulk genomic and transcriptomic profiles of 765 liver tumors. Our results offer insight into the diverse ecosystem of liver cancer and its impact on patient prognosis.
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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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                Author and article information

                Contributors
                Liwu Fu: Fulw@mail.sysu.edu.cn
                Xianwei Wang: Wangxianwei1116@126.com
                Journal
                Journal ID (nlm-ta): Mol Cancer
                Journal ID (iso-abbrev): Mol. Cancer
                Title: Molecular Cancer
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1476-4598
                Publication date (Electronic): 14 March 2020
                Publication date PMC-release: 14 March 2020
                Publication date Collection: 2020
                Volume: 19
                Electronic Location Identifier: 58
                Affiliations
                [1 ]GRID grid.412990.7, ISNI 0000 0004 1808 322X, Henan Key Laboratory of Medical Tissue Regeneration, College of Basic Medical Sciences, , Xinxiang Medical University, ; Xinxiang, Henan China
                [2 ]GRID grid.412990.7, ISNI 0000 0004 1808 322X, School of Laboratory Medicine, , Xinxiang Medical University, ; Xinxiang, Henan China
                [3 ]GRID grid.488530.2, ISNI 0000 0004 1803 6191, State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, , Sun Yat-sen University Cancer Center, ; Guangzhou, China
                Article
                Publisher ID: 1180
                DOI: 10.1186/s12943-020-01180-y
                PMC ID: 7071709
                PubMed ID: 32171304
                SO-VID: 09c6daca-309d-4407-9908-4ae003dcd521
                Copyright © © The Author(s) 2020
                License:

                Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

                History
                Date received : 9 December 2019
                Date accepted : 5 March 2020
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: circrnas,cancer therapy,sensitivity,radioresistance,chemoresistance,multidrug resistance
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: circrnas, cancer therapy, sensitivity, radioresistance, chemoresistance, multidrug resistance

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