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      Circular RNA MYLK serves as an oncogene to promote cancer progression via microRNA-195/cyclin D1 axis in laryngeal squamous cell carcinoma

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          Abstract

          Laryngeal squamous cell carcinoma (LSCC) is a common aggressive head and neck cancer. Circular RNAs (circRNAs) are implicated in numerous physiological and pathological processes, including tumorigenesis. The present study aimed to investigate the expression profile and biological role of circMYLK in LSCC. We found that circMYLK was highly expressed in LSCC tissues and cell lines. circMYLK overexpression promoted LSCC cell proliferation and G 1/S cell cycle transition; whereas circMYLK knockdown had the contrary effects. Mechanistically, circMYLK can serve as a competing endogenous RNA for miR-195 to increase cyclin D1 expression in LSCC, and rescue experiments further showed that restoration of miR-195 could block the oncogenic role of circMYLK in LSCC. In conclusion, our findings indicate that the circMYLK/miR-195/cyclin D1 regulatory axis could affect the proliferation and cell cycle progression of LSCC cells, and may provide a novel therapeutic target for the treatment of LSCC.

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          CDR1as is overexpressed in laryngeal squamous cell carcinoma to promote the tumour’s progression via miR-7 signals

          Jianzhong Zhang, Huayong Hu, Yaoxin Zhao … (2018)
          To investigate the roles played by the circular RNA (circRNA) molecule ciRS‑7 (CDR1as) and tumour suppressor miRNA‐7 (miR‐7) in laryngeal squamous cell carcinoma (LSCC). Specimens of LSCC tissue (n = 30) and corresponding relative normal tissue (n = 30) were collected to determine their levels and clinical significance of CDR1as/mir‐7 expression. The CDR1as and miR‐7 were overexpressed in LSCC cells to investigate its function and mechanism in vitro and in vivo. Patients with high TNM stages, poorly differentiated tumours, lymph node metastases and poor prognosis had high CDR1as levels but low miR‐7 levels. CDR1 expression was negatively associated with miR‐7 expression in LSCC. Overexpression of CDR1as in vitro enhanced cell vitality, and promoted the proliferation, migration, and invasion of two LSCC cell lines (Hep2 and AMC‐HN‐8.) However, these effects could be abrogated by knockdown of CDR1as or the forced expression of miR‐7. Mechanistically, overexpressed CDR1 molecules functioned as miR‐7 sponges and upregulated the key targets of miR‐7, CCNE1, and PIK3CD in Hep2 and AMC‐HN‐8 cells. In vivo studies demonstrated the tumourigenic role of CDR1as. Overexpression of CDR1as alone promoted tumour growth and increased expression of the proliferation indices ki‐67, CCNE1, and PIK3CD. Although the tumour suppressor miR‐7 effectively inhibited the tumour growth, this effect could be counteracted by co‐treatment with CDR1as in vivo. CDR1as is an oncogene that promotes LSCC progression by regulating miR‐7 signals.
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            Circular RNA Myosin Light Chain Kinase (MYLK) Promotes Prostate Cancer Progression through Modulating Mir-29a Expression

            Yuanqing Dai, Dongjie Li, Xiong Chen … (2018)
            Background In developed countries, prostate cancer (PCa) is a frequently diagnosed cancer with the second highest fatality rate. Circular RNAs (circRNAs) are a class of endogenous non-coding RNAs (ncRNAs) stably expressed in cells and involved in a series of carcinomas. However, few research studies have reported on the role of circRNAs in PCa. Material/Methods We used qRT-PCR to detect the expression of circMYLK (circRNA ID: hsa_circ_0141940) and miR-29a in PCa tissues and cell lines. MTT, colony formation, and TUNEL assays were performed to analysis the cell viability of PCa cells. Transwell and wound scratch assays were performed to investigate the cell invasion and migration of PCa cells. Results In the present study, we confirmed that circMYLK expression level was significantly higher in PCa samples and PCa cells than in normal tissues and normal prostatic cells. The upregulated circRNA-MYLK promoted PCa cells proliferation, invasion, and migration; however, si-circRNA-MYLK significantly accelerated the PCa cell apoptosis. We also observed that the aforementioned function of circRNA-MYLK on PCa cells was affected through targeting miR-29a. Conclusions We confirmed circRNA-MYLK was an oncogene in PCa and revealed a novel mechanism underlying circRNA-MYLK in PC progression.
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              Circular RNAs and competing endogenous RNA (ceRNA) networks

              Apratim Mitra, Karl Pfeifer, Ki-Sun Park (2018)
              In recent years, advances in bioinformatics approaches have allowed a systematic characterization of circular RNAs (circRNAs) across a variety of cell types. Demonstration of cell type specificity, regulated expression, and conservation between species all suggest that circRNAs have functional importance. Especially, investigators have begun focusing on the possibility that circRNAs operate as part of competing endogenous RNA (ceRNA) regulatory networks that are proposed to play critical roles in normal development and in pathologic conditions like cancer.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Biosci Rep
                Journal ID (iso-abbrev): Biosci. Rep
                Journal ID (hwp): ppbioscirep
                Journal ID (publisher-id): BSR
                Title: Bioscience Reports
                Publisher: Portland Press Ltd.
                ISSN (Print): 0144-8463
                ISSN (Electronic): 1573-4935
                Publication date (Electronic preprint): 19 August 2019
                Publication date Collection: 30 September 2019
                Publication date (Electronic): 03 September 2019
                Volume: 39
                Issue: 9
                Electronic Location Identifier: BSR20190227
                Affiliations
                [1 ]Department of Otorhinolaryngology Head and Neck, Affiliated Hospital of Hebei Engineering University, Handan 056002, Hebei Province, China
                [2 ]Department of Otorhinolaryngology Head and Neck, The 4th Central Hospital of Tianjin, Tianjin 300140, China
                [3 ]Department of Anesthesia, Affiliated Hospital of Hebei Engineering University, Handan 056002, Hebei Province, China
                [4 ]Department of Neurology, Affiliated Hospital of Hebei Engineering University, Handan 056002, Hebei Province, China
                [5 ]Department of Neurosurgery, Affiliated Hospital of Hebei Engineering University, Handan 056002, Hebei Province, China
                [6 ]Department of Aesthetic Plastic Surgery, Affiliated Hospital of Hebei Engineering University, Handan 056002, Hebei Province, China
                Author notes
                Correspondence: Zhihai Zhai ( dr_zhaizhihai66@ 123456163.com )
                Author information
                http://orcid.org/0000-0002-0749-7086
                Article
                DOI: 10.1042/BSR20190227
                PMC ID: 6722494
                PubMed ID: 31427478
                SO-VID: 2c2cbf6f-34c7-499e-b559-f290efce86f7
                Copyright © © 2019 The Author(s).
                License:

                This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).

                History
                Date received : 26 January 2019
                Date revision received : 03 July 2019
                Date accepted : 01 August 2019
                Page count
                Pages: 8
                Categories
                Subject: Research Articles
                Subject: Research Article
                Subject: 39
                Subject: 46
                Subject: 10

                ScienceOpen disciplines: Life sciences
                Keywords: cell cycle,circular rna mylk,cyclin d1,laryngeal squamous cell carcinoma,microrna-195
                Data availability:
                ScienceOpen disciplines: Life sciences
                Keywords: cell cycle, circular rna mylk, cyclin d1, laryngeal squamous cell carcinoma, microrna-195

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