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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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      Long Non-Coding RNA-NEAT1 Promotes Cell Migration and Invasion via Regulating miR-124/NF-κB Pathway in Cervical Cancer

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          This study aimed to investigate the regulatory role of lncRNA-NEAT1 on cervical cancer (CC) and the underlying molecular mechanisms.

          Methods

          The expression of lncRNA-NEAT1 and miR-124 was detected in CC tissues and cells (HeLa and SiHa cells) by qRT-RCR. The relation between lncRNA-NEAT1 expression and clinical parameters of CC patients was explored. The cell migration and invasion were detected by wound healing assay and transwell assay. The cell proliferation was detected by CCK-8 and anchorage-independent colony assay. The targeting relation between miR-124 and lncRNA-NEAT1 was predicted by TargetScan and identified by dual luciferase reporter gene and RNA pull-down assay. The expression of metastasis- (MMP-2 and MMP), EMT- (E-cadherin, N-cadherin and Vimentin), and NF-κB pathway-related factors (NF-κB p65, p-NF-κB p65 and IκBα) was detected by Western blot.

          Results

          The expression of lncRNA-NEAT1 was upregulated in CC tissues and cells and positively correlated with TNM stage and lymph node metastasis. Overexpression of lncRNA-NEAT1 promoted the proliferation, migration and invasion, influenced the expression of EMT markers, and activated NF-κB pathway in HeLa and SiHa cells. Silencing of lncRNA-NEAT1 exhibited opposite effects on HeLa and SiHa cells. LncRNA-NEAT1 could negatively regulate its target miR-124. MiR-124 reversed the effects of lncRNA-NEAT1 on the migration, invasion, EMT and NF-κB pathway of HeLa cells.

          Conclusion

          LncRNA-NEAT1 promoted the migration and invasion of CC cells via regulating miR-124/NF-κB pathway.

          Most cited references23

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          Long non-coding RNAs: potential new biomarkers for predicting tumor invasion and metastasis

          Long non-coding RNAs (lncRNAs) play important roles in malignant neoplasia. Indeed, many hallmarks of cancer define that the malignant phenotype of tumor cells are controlled by lncRNAs. Despite a growing number of studies highlighting their importance in cancer, there has been no systematic review of metastasis-associated lncRNAs in various cancer types. Accordingly, we focus on the key metastasis-related lncRNAs and outline their expression status in cancer tissues by reviewing the previous stuides, in order to summarize the nowadays research achivements for lncRNAs related to cancer metastasis. Medline, EMBASE, as well as PubMed databases were applied to study lncRNAs which were tightly associated with tumor invasion and metastasis. Up to now, a substantial number of lncRNAs have been found to have important biological functions. In this review, according to their various features in cancer, lncRNAs were roughly divided into three categories: promoting tumor invasion and metastasis, negative regulation of tumor metastasis and with dual regulatory roles. The present studies may establish the foundation for both further research on the mechanisms of cancer progression and future lncRNA-based clinical applications.
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            The lncRNA NEAT1 facilitates cell growth and invasion via the miR-211/HMGA2 axis in breast cancer.

            Long non-coding RNAs play a significant role in cancer metastasis. Studies have demonstrated that LncRNA NEAT1 promotes cancer progression. We aimed to explore whether NEAT1 regulated growth and invasion in breast cancer cells. We provided evidence that lncRNA NEAT1 was up-regulated in breast cancer cell lines and tissues. NEAT1 promoted invasion through inducing Epithelial-mesenchymal transition (EMT) and NEAT1 played a role in 5-fluorouracil (5-FU) resistance. In addition, we revealed a reciprocal repression between NEAT1 and miR-211. Furthermore, the EMT-inducer HMGA2 was identified as a down-stream target of miR-211. LncRNA NEAT1 induced EMT and 5-FU resistance through the miR-211/HMGA2 axis. Our findings suggest that lncRNA NEAT1 could be a new diagnostic biomarker and therapy target for breast cancer.
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              MiR-34a Promotes Apoptosis and Inhibits Autophagy by Targeting HMGB1 in Acute Myeloid Leukemia Cells.

              MiR-34a is identified as a tumor suppressor gene and involved in acute myeloid leukemia (AML) development. However, the regulatory mechanism of miR-34a in AML is unclear.
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                Author and article information

                Journal
                Onco Targets Ther
                Onco Targets Ther
                OTT
                ott
                OncoTargets and therapy
                Dove
                1178-6930
                17 April 2020
                2020
                : 13
                : 3265-3276
                Affiliations
                [1 ]Department of Obstetrics-Gynecology, Dongying City People’s Hospital , Dongying City, Shandong Province 257091, People’s Republic of China
                [2 ]Department of Obstetrics-Gynecology, Dongying City Dongying District People’s Hospital , Dongying City, Shandong Province 257000, People’s Republic of China
                Author notes
                Correspondence: Xiaofang Shen Department of Obstetrics-Gynecology, Dongying City People’s Hospital , No. 317, Nanyi Road, Dongying District, Dongying City, Shandong Province257091, People’s Republic of ChinaTel +86-13780757608 Email shenxiaofang142@163.com
                [*]

                These authors contributed equally to this work

                Author information
                http://orcid.org/0000-0002-0392-7288
                Article
                220306
                10.2147/OTT.S220306
                7173957
                32368085
                771e0ae3-3fc9-44df-bde9-f8334c43083c
                © 2020 Shen 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                : 21 June 2019
                : 26 March 2020
                Page count
                Figures: 7, Tables: 1, References: 37, Pages: 12
                Categories
                Original Research

                Oncology & Radiotherapy
                cervical cancer,lncrna-neat1,migration,invasion,mir-124/nf-κb pathway
                Oncology & Radiotherapy
                cervical cancer, lncrna-neat1, migration, invasion, mir-124/nf-κb pathway

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