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      LINC01094 triggers radio-resistance in clear cell renal cell carcinoma via miR-577/CHEK2/FOXM1 axis

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          Abstract

          Background

          Radioresistance is an obstacle to limit efficacy of radiotherapy. Meanwhile, long non-coding RNAs (lncRNAs) have been reported to affect radioresistance. Here, we aimed to investigate lncRNAs involving radioresistance development of clear cell renal cell carcinoma (ccRCC), the most frequent type of renal cell carcinoma (RCC).

          Methods

          The mRNA and protein expressions of genes were measured via qRT-PCR and western blot. The relationships among genes were verified by RIP and luciferase reporter assay. The radioresistance of ccRCC cells was evaluated through clonogenic survival assay, MTT assay and TUNEL assay.

          Results

          LINC01094 was over-expressed in ccRCC cell lines. LINC01094 expression was increased along with the radiation exposure time and the final stable level was 8 times of the initial level. Knockdown of LINC01094 resulted in enhanced radiosensitivity of ccRCC cells. Mechanically, LINC01094 was a ceRNA of CHEK2 by sponging miR-577. Also, the enhancement of LINC01094 on ccRCC radioresistance was mediated by CHEK2-stabilized FOXM1 protein.

          Conclusion

          LINC01094 facilitates ccRCC radioresistance by targeting miR-577/CHEK2/FOXM1 axis, blazing a new trail for overcoming radioresistance in ccRCC.

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          Most cited references22

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          DNA double-strand breaks: signaling, repair and the cancer connection.

          K K Khanna, S P Jackson, Stefan Kubicek … (2001)
          To ensure the high-fidelity transmission of genetic information, cells have evolved mechanisms to monitor genome integrity. Cells respond to DNA damage by activating a complex DNA-damage-response pathway that includes cell-cycle arrest, the transcriptional and post-transcriptional activation of a subset of genes including those associated with DNA repair, and, under some circumstances, the triggering of programmed cell death. An inability to respond properly to, or to repair, DNA damage leads to genetic instability, which in turn may enhance the rate of cancer development. Indeed, it is becoming increasingly clear that deficiencies in DNA-damage signaling and repair pathways are fundamental to the etiology of most, if not all, human cancers. Here we describe recent progress in our understanding of how cells detect and signal the presence and repair of one particularly important form of DNA damage induced by ionizing radiation-the DNA double-strand break (DSB). Moreover, we discuss how tumor suppressor proteins such as p53, ATM, Brca1 and Brca2 have been linked to such pathways, and how accumulating evidence is connecting deficiencies in cellular responses to DNA DSBs with tumorigenesis.
          Article 0 comments Cited 560 times – based on 0 reviews     Review now
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            Exploring the role of cancer stem cells in radioresistance.

            Michael Baumann, Mechthild Krause, Richard Hill (2008)
            Radiobiological research over the past decades has provided evidence that cancer stem cell content and the intrinsic radiosensitivity of cancer stem cells varies between tumours, thereby affecting their radiocurability. Translation of this knowledge into predictive tests for the clinic has so far been hampered by the lack of methods to discriminate between stem cells and non-stem cells. New technologies allow isolation of cells expressing specific surface markers that are differentially expressed in tumour cell subpopulations that are enriched for cancer stem cells. Combining these techniques with functional radiobiological assays holds the potential to elucidate the role of cancer stem cells in radioresistance in individual tumours, and to use this knowledge for the development of predictive markers for optimization of radiotherapy.
            Article 0 comments Cited 240 times – based on 0 reviews     Review now
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              Ionizing radiation-induced DNA damage, response, and repair.

              Wil L. Santivasi, Fen Xia (2014)
              Ionizing radiation (IR) is an effective and commonly employed treatment in the management of more than half of human malignancies. Because IR's ability to control tumors mainly relies on DNA damage, the cell's DNA damage response and repair (DRR) processes may hold the key to determining tumor responses. IR-induced DNA damage activates a number of DRR signaling cascades that control cell cycle arrest, DNA repair, and the cell's fate. DNA double-strand breaks (DSBs) generated by IR are the most lethal form of damage, and are mainly repaired via either homologous recombination (HR) or nonhomologous end-joining (NHEJ) pathways.
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                Author and article information

                Contributors
                Yufeng Jiang: 897986343@qq.com
                Wei Li: liweitongji@163.com
                Yang Yan: 13564368328@163.com
                Xudong Yao: yaoxudong67@sina.com
                Wenyu Gu: guwenyu1234@126.com
                Haimin Zhang:
                ORCID: http://orcid.org/0000-0002-2134-3120
                zhm1064@163.com
                Journal
                Journal ID (nlm-ta): Cancer Cell Int
                Journal ID (iso-abbrev): Cancer Cell Int
                Title: Cancer Cell International
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1475-2867
                Publication date (Electronic): 24 June 2020
                Publication date PMC-release: 24 June 2020
                Publication date Collection: 2020
                Volume: 20
                Electronic Location Identifier: 274
                Affiliations
                [1 ]GRID grid.24516.34, ISNI 0000000123704535, Department of Urology, Chongming Branch, Shanghai Tenth People’s Hospital, , Tongji University School of Medicine, ; No.66 Xiangyang Road, Chongming District, Shanghai, 202157 China
                [2 ]GRID grid.24516.34, ISNI 0000000123704535, Department of Urology, Shanghai Tenth People’s Hospital, , Tongji University School of Medicine, ; No.301 Yanchang Road, Jing’an District, Shanghai, 200072 China
                Author information
                http://orcid.org/0000-0002-2134-3120
                Article
                Publisher ID: 1306
                DOI: 10.1186/s12935-020-01306-8
                PMC ID: 7315499
                PubMed ID: 32595418
                SO-VID: 51b5ebfa-2ad0-4854-9826-938a292ebccb
                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 : 11 July 2019
                Date accepted : 28 May 2020
                Funding
                Funded by: The Project of Scientific Research Topic of Shanghai Municipal Health and Family Planning Commission: “The Effect of BX649059's Interaction with microRNA on the Occurrence and Development of Renal Cancer and Its Molecular Mechanism”
                Award ID: 201640146
                Award Recipient :
                Categories
                Subject: Primary Research
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: linc01094,ccrcc radio-resistance,mir-577,chek2,foxm1
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: linc01094, ccrcc radio-resistance, mir-577, chek2, foxm1

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