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      OncoTargets and Therapy (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on the pathological basis of cancers, potential targets for therapy and treatment protocols to improve the management of cancer patients. Publishing high-quality, original research on molecular aspects of cancer, including the molecular diagnosis, since 2008. Sign up for email alerts here. 50,877 Monthly downloads/views I 4.345 Impact Factor I 7.0 CiteScore I 0.81 Source Normalized Impact per Paper (SNIP) I 0.811 Scimago Journal & Country Rank (SJR)

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      lncRNA PCAT6 promotes non-small cell lung cancer cell proliferation, migration and invasion through regulating miR-330-5p

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          Abstract

          Background

          Investigating the roles of lncRNA prostate cancer-associated transcript 6 (PCAT6) in modulating the growth and aggressiveness of non-small-cell lung carcinoma (NSCLC) cell.

          Method

          The levels of PCAT6 in NSCLC tissues and cell lines were determined by quantitative real-time PCR assay. MTT as well as colony formation assays were applied to explore the effect of PCAT6 on the growth of NSCLC cell in vitro. Wound healing and Transwell assays were utilized to analyze the impact of PCAT6 on the migration and invasion of NSCLC cell. Bioinformatics analysis and luciferase reporter assay were used to prove that miR-330-5p was the target of PCAT6. Colony formation, wound healing, and Transwell invasion assays were applied to demonstrate that PCAT6 promoted NSCLC cell growth, migration, and invasion through binding miR-330-5p. Finally, xenograft model was used to explore the role of PCAT6 in the tumor growth of NSCLC cell in vivo.

          Results

          PCAT6 was highly overexpressed in NSCLC tissues and cells compared with normal tissues and non-tumorigenic bronchial epithelial cell line, BEAS-2B. Downregulation of PCAT6 markedly reduced the proliferation, migration, and invasion of NSCLC cell. Moreover, down-expression of PCAT6 significantly increased the level of miR-330-5p in NSCLC cell. Further functional experiments indicated that down-expression of miR-330-5p reversed the inhibitory effect of PCAT6 on NSCLC cell growth, migration, and invasion.

          Conclusion

          Our results reveal that lncRNA PCAT6 facilitates the proliferation, migration, and invasion of NSCLC cell via competitively binding to miR-330-5p.

          Most cited references20

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          Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

          Summary Long noncoding RNAs (lncRNAs) are commonly dysregulated in tumors, but only a handful are known to play pathophysiological roles in cancer. We inferred lncRNAs that dysregulate cancer pathways, oncogenes, and tumor suppressors (cancer genes) by modeling their effects on the activity of transcription factors, RNA-binding proteins, and microRNAs in 5,185 TCGA tumors and 1,019 ENCODE assays. Our predictions included hundreds of candidate onco- and tumor-suppressor lncRNAs (cancer lncRNAs) whose somatic alterations account for the dysregulation of dozens of cancer genes and pathways in each of 14 tumor contexts. To demonstrate proof of concept, we showed that perturbations targeting OIP5-AS1 (an inferred tumor suppressor) and TUG1 and WT1-AS (inferred onco-lncRNAs) dysregulated cancer genes and altered proliferation of breast and gynecologic cancer cells. Our analysis indicates that, although most lncRNAs are dysregulated in a tumor-specific manner, some, including OIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergistically dysregulate cancer pathways in multiple tumor contexts.
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            Long non-coding RNA SNHG1 regulates NOB1 expression by sponging miR-326 and promotes tumorigenesis in osteosarcoma

            The long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been demonstrated to participate in the deterioration of many types of cancer. However, the underlying mechanisms of SNHG1-mediating functions in osteosarcoma (OS) have yet to be elucidated. In the present study, our results showed that SNHG1 was upregulated in OS tissues and cell lines, and high SNHG1 expression predicts poor overall survival of OS patients. Knockdown of SNHG1 inhibited cell growth and metastasis of OS in vitro and in vivo. Furthermore, our data demonstrated that there was reciprocal repression between SNHG1 and miR-326 which act as a tumor suppressor in OS cells, and exhibiting a strong negative relationship between SNHG1 and miR-326 expression in OS tissues. Additionally, we identified that SNHG1 increased human nin one binding protein (NOB1), an oncogene, through sponging miR-326 as competing endogenous RNA (ceRNA), finally prompting cell growth, migration and invasion in OS. Collectively, these findings not only uncovered that the SNHG1/miR-326/NOB1 signaling axis has a key role in OS progression but also suggested the potential application of SNHG1 and miR-326 as biomarkers in the OS diagnosis and treatment.
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              Analysis of the miRNA–mRNA–lncRNA network in human estrogen receptor-positive and estrogen receptor-negative breast cancer based on TCGA data

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                Author and article information

                Journal
                Onco Targets Ther
                Onco Targets Ther
                OncoTargets and Therapy
                OncoTargets and therapy
                Dove Medical Press
                1178-6930
                2018
                01 November 2018
                : 11
                : 7715-7724
                Affiliations
                [1 ]Department of Oncology, People’s Hospital of Jingjiang, Jingjiang, China, yulijiangylj@ 123456hainan.net
                [2 ]Department of Oncology, The Northern Jiangsu People’s Hospital, Yangzhou, China
                Author notes
                Correspondence: Li Jiang Yu, Department of Oncology, People’s Hospital of Jingjiang, No 28 Zhongzhou Road, Jingjiang, Jiangsu 214500, China, Tel +86 523 8499 6506, Email yulijiangylj@ 123456hainan.net
                Article
                ott-11-7715
                10.2147/OTT.S178597
                6219114
                30464520
                141604e1-cabd-4356-a599-ba7f89554de8
                © 2018 Cui et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Oncology & Radiotherapy
                pcat6,mir-330-5p,nsclc,growth,migration,invasion
                Oncology & Radiotherapy
                pcat6, mir-330-5p, nsclc, growth, migration, invasion

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