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      DANCR‐mediated microRNA‐665 regulates proliferation and metastasis of cervical cancer through the ERK/SMAD pathway

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          Abstract

          Emerging evidence has indicated that microRNAs (mi RNAs) play an important role in cervical cancer ( CC). However, the role of miRNA (miR)‐665 in cervical cancer remains unclear. The aim of the present study was to investigate the potential functions of miR‐665 in CC and to identify the underlying mechanisms of action. Herein, we show that miR‐665 was downregulated in CC tissues and cell lines, which is negatively correlated with tumor size, distant metastasis, advanced TNM stage and poor prognosis. Functionally, miR‐665 inhibited cell proliferation, migration and invasion and resistance of cisplatin for CC cells, as well as tumor growth. We validated that transforming growth factor beta receptor 1 ( TGFBR1) was a direct target of miR‐665 and mediated the ERK/ SMAD pathway. In addition, we identified miR‐665 as the competing endogenous RNA for long noncoding (lnc)‐ DANCR. These observations suggested that lnc‐ DANCR‐mediated miR‐665 downregulation regulates the malignant phenotype of CC cells by targeting TGFBR1 through the ERK/ SMAD pathway, which may present a pathway for novel therapeutic stratagems for CC therapy.

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          Long noncoding RNA DANCR, working as a competitive endogenous RNA, promotes ROCK1-mediated proliferation and metastasis via decoying of miR-335-5p and miR-1972 in osteosarcoma

          Yong Wang, Xiandong Zeng, Ningning Wang … (2018)
          Background Accumulating evidences indicate that non-coding RNAs (ncRNAs) including long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) acting as crucial regulators in osteosarcoma (OS). Previously, we reported that Rho associated coiled-coil containing protein kinase 1 (ROCK1), a metastatic-related gene was negatively regulated by microRNA-335-5p (miR-335-5p) and work as an oncogene in osteosarcoma. Whether any long non-coding RNAs participate in the upstream of miR-335-5p/ROCK1 axial remains unclear. Methods Expression of differentiation antagonizing non-protein coding RNA (DANCR) and miR-335-5p/miR-1972 in osteosarcoma tissues were determined by a qRT-PCR assay and an ISH assay. Osteosarcoma cells’ proliferation and migration/invasion ability changes were measured by a CCK-8/EDU assay and a transwell assay respectively. ROCK1 expression changes were checked by a qRT-PCR assay and a western blot assay. Targeted binding effects between miR-335-5p/miR-1972 and ROCK1 or DANCR were verified by a dual luciferase reporter assay and a RIP assay. In vivo experiments including a nude formation assay as well as a CT scan were applied to detect tumor growth and metastasis changes in animal level. Results In the present study, an elevated DNACR was found in osteosarcoma tissue specimens and in osteosarcoma cell lines, and the elevated DNACR was closely correlated with poor prognosis in clinical patients. Functional experiments illustrated that a depression of DANCR suppressed ROCK1-mediated proliferation and metastasis in osteosarcoma cells. The results of western blot assays and qRT-PCR assays revealed that DANCR regulated ROCK1 via crosstalk with miR-335-5p and miR-1972. Further cellular behavioral experiments demonstrated that DNACR promoted ROCK1-meidated proliferation and metastasis through decoying both miR-335-5p and miR-1972. Finally, the outcomes of in vivo animal models showed that DANCR promoted tumor growth and lung metastasis of osteosarcoma. Conclusions LncRNA DANCR work as an oncogene and promoted ROCK1-mediated proliferation and metastasis through acting as a competing endogenous RNA (ceRNA) in osteosarcoma. Electronic supplementary material The online version of this article (10.1186/s12943-018-0837-6) contains supplementary material, which is available to authorized users.
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            LncRNA DANCR Promotes Lung Cancer by Sequestering miR-216a

            Qiang Zhen, Li-na Gao, Ren-feng Wang … (2018)
            Background: Long noncoding RNAs (lncRNAs) are a new class of cancer regulators. Here, we aimed to investigate the diagnostic and therapeutic values of an lncRNA, differentiation antagonizing noncoding RNA (DANCR), in lung cancer. Methods: Real-time polymerase chain reaction was used to compare DANCR levels in normal and cancerous lung tissues as well as lung cancer cells. Lentiviral transduction was used to induce DANCR overexpression or silencing in vitro, followed by monitoring cell proliferation, colony formation, and changes in microRNA-216a (miR-216a) expression. DANCR-specific small hairpin RNA transduction was used to establish cells with stable DANCR knockdown, and silenced cells were used to initiate lung tumor xenografts, followed by monitoring tumor growth. Results: DANCR upregulation was seen in lung cancer, particularly in high-grade lung cancer tissues and aggressive cancer cells. Ectopic DANCR expression induced lung cancer cell proliferation and colony formation, whereas DANCR silencing induced opposing effects. The miR-216a level in cancer cells was negatively correlated with DANCR expression. The DANCR knockdown reduced the growth of tumor xenografts in vivo. Conclusion: DANCR upregulation is a potential indicator of aggressive lung cancer. Silencing of DANCR has great potential as a potent therapeutic strategy in lung cancer.
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              Exosomal miR-665 as a novel minimally invasive biomarker for hepatocellular carcinoma diagnosis and prognosis

              Zhen Qu, Junhua Wu, Junyi Wu … (2017)
              Recent studies have shown that circulating microRNAs are potential biomarkers for various types of malignancies. The aim of this study was to investigate the feasibility of using serum exosomal microRNAs (miRNAs) as novel serological biomarkers for hepatocellular carcinoma (HCC) diagnosis and prognosis. Exosomes are small membranous vesicles (30–100 nm). Exosomal miR-665 levels in HCC patients were significantly higher than those in healthy subjects (P 5 cm), in tumours with local invasion and in those at an advanced clinical stage (stage III/IV) of HCC (P = 0.0042, 0.0197, and 0.0276, respectively). The survival time of the exosomal miR-665 high-expression group (n = 17) was significantly shorter than that of the low-expression group (n = 13) (P = 0.036). In addition, we found that HCC cell-derived exosomes promoted hepatoma cell proliferation and upregulated the expression level of proteins in the MAPK/ERK pathway in vitro and in vivo. This study suggests that serum exosomal miR-665 may be a novel minimally invasive biomarker for HCC diagnosis and prognosis.
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                Author and article information

                Contributors
                Lixin Dong:
                ORCID: https://orcid.org/0000-0002-0241-8959
                donglixin6447@sina.com
                Journal
                Journal ID (nlm-ta): Cancer Sci
                Journal ID (iso-abbrev): Cancer Sci
                Journal ID (doi): 10.1111/(ISSN)1349-7006
                Journal ID (publisher-id): CAS
                Title: Cancer Science
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1347-9032
                ISSN (Electronic): 1349-7006
                Publication date (Electronic): 19 January 2019
                Publication date (Print): March 2019
                Volume: 110
                Issue: 3 ( doiID: 10.1111/cas.2019.110.issue-3 )
                Pages: 913-925
                Affiliations
                [ 1 ] Department of Radiation Oncology The First Hospital of Qinhuangdao Qinhuangdao China
                [ 2 ] Department of Gynecology The First Hospital of Qinhuangdao Qinhuangdao China
                [ 3 ] Department of Gastroenterology The First Hospital of Qinhuangdao Qinhuangdao China
                Author notes
                [*] [* ] Correspondence

                Lixin Dong, Department of Radiation Oncology, The First Hospital of Qinhuangdao, Qinhuangdao, China.

                Email: donglixin6447@ 123456sina.com

                Author information
                https://orcid.org/0000-0002-0241-8959
                Article
                Publisher ID: CAS13921
                DOI: 10.1111/cas.13921
                PMC ID: 6398927
                PubMed ID: 30582654
                SO-VID: eb7ca186-3c74-4b70-90ae-ae6b43b40a7e
                Copyright © © 2018 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date received : 04 September 2018
                Date revision received : 11 December 2018
                Date accepted : 18 December 2018
                Page count
                Figures: 6, Tables: 1, Pages: 13, Words: 6878
                Funding
                Funded by: Science and Technology Research and Development Plan of Hebei
                Award ID: 162777146
                Categories
                Subject: Original Article
                Subject: Original Articles
                Subject: Carcinogenesis
                Custom metadata
                source-schema-version-number 2.0
                component-id cas13921
                cover-date March 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.1 mode:remove_FC converted:04.03.2019

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cervical cancer,dancr,erk/smad,mir‐665,tgfbr1
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cervical cancer, dancr, erk/smad, mir‐665, tgfbr1

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