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      EPEL promotes the migration and invasion of osteosarcoma cells by upregulating ROCK1

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          Abstract

          E2F-mediated cell proliferation enhancing long non-coding RNA (lncRNA) (EPEL) is a newly identified lncRNA involved in the regulation of lung cancer cell proliferation. However, its association with other types of cancer is unknown. The present study recruited patients with osteosarcoma and healthy controls. Tumor and adjacent healthy tissues were obtained from patients with osteosarcoma, and whole blood was extracted from patients and healthy controls. The expression levels of EPEL in tissues were detected by reverse transcription-quantitative polymerase chain reaction. The diagnostic value of serum EPEL for osteosarcoma was evaluated by receiver operating characteristic curve analysis. The association between serum levels of EPEL and basic clinical patient information was analyzed by χ 2 test. Subsequently, EPEL overexpression in osteosarcoma cell lines was established, and its effects on cell migration and invasion were explored by Transwell assay. The implications of EPEL overexpression on Rho-associated coiled-coil containing protein kinase 1 (ROCK1) expression were investigated by western blotting. The results revealed that EPEL was upregulated in tumor tissues compared with adjacent tissues. In addition, serum levels of EPEL were higher in patients with osteosarcoma compared with healthy controls, and were positively associated with distant tumor metastasis. Furthermore, EPEL overexpression promoted the migration and invasion of osteosarcoma cells and induced overexpression of ROCK1. In conclusion, these results suggested that EPEL may promote the migration and invasion of osteosarcoma cells by upregulating ROCK1.

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          miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer

          Background microRNAs have been established as powerful regulators of gene expression in normal physiological as well as in pathological conditions, including cancer progression and metastasis. Recent studies have demonstrated a key role of miR-31 in the progression and metastasis of breast cancer. Downregulation of miR-31 enhances several steps of the invasion-metastasis cascade in breast cancer, i.e., local invasion, extravasation and survival in the circulation system, and metastatic colonization of distant sites. miR-31 exerts its metastasis-suppressor activity by targeting a cohort of pro-metastatic genes, including RhoA and WAVE3. The molecular mechanisms that lead to the loss of miR-31 and the activation of its pro-metastatic target genes during these specific steps of the invasion-metastasis cascade are however unknown. Results In the present report, we identify promoter hypermethylation as one of the major mechanisms for silencing miR-31 in breast cancer, and in the triple-negative breast cancer (TNBC) cell lines of basal subtype, in particular. miR-31 maps to the intronic sequence of a novel long non-coding (lnc)RNA, LOC554202 and the regulation of its transcriptional activity is under control of LOC554202. Both miR-31 and the host gene LOC554202 are down-regulated in the TNBC cell lines of basal subtype and over-expressed in the luminal counterparts. Treatment of the TNBC cell lines with either a de-methylating agent alone or in combination with a de-acetylating agent resulted in a significant increase of both miR-31 and its host gene, suggesting an epigenetic mechanism for the silencing of these two genes by promoter hypermethylation. Finally, both methylation-specific PCR and sequencing of bisulfite-converted DNA demonstrated that the LOC554202 promoter-associated CpG island is heavily methylated in the TNBC cell lines and hypomethylated in the luminal subtypes. Conclusion Loss of miR-31 expression in TNBC cell lines is attributed to hypermethylation of its promoter-associated CpG island. Together, our results provide the initial evidence for a mechanism by which miR-31, an important determinant of the invasion metastasis cascade, is regulated in breast cancer.
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            Lnc2Cancer: a manually curated database of experimentally supported lncRNAs associated with various human cancers

            Lnc2Cancer (http://www.bio-bigdata.net/lnc2cancer) is a manually curated database of cancer-associated long non-coding RNAs (lncRNAs) with experimental support that aims to provide a high-quality and integrated resource for exploring lncRNA deregulation in various human cancers. LncRNAs represent a large category of functional RNA molecules that play a significant role in human cancers. A curated collection and summary of deregulated lncRNAs in cancer is essential to thoroughly understand the mechanisms and functions of lncRNAs. Here, we developed the Lnc2Cancer database, which contains 1057 manually curated associations between 531 lncRNAs and 86 human cancers. Each association includes lncRNA and cancer name, the lncRNA expression pattern, experimental techniques, a brief functional description, the original reference and additional annotation information. Lnc2Cancer provides a user-friendly interface to conveniently browse, retrieve and download data. Lnc2Cancer also offers a submission page for researchers to submit newly validated lncRNA-cancer associations. With the rapidly increasing interest in lncRNAs, Lnc2Cancer will significantly improve our understanding of lncRNA deregulation in cancer and has the potential to be a timely and valuable resource.
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              Recent advances in osteosarcoma.

              Although osteosarcoma (OS) is a rare malignancy, it is ranked among the leading causes of cancer-related death in the pediatric age group. The cancer's low prevalence and its large tumor heterogeneity make it difficult to obtain meaningful progress in patient survival. In this review we present an overview of current clinical trials which largely focus on stimulation of the immune system or rely on the inhibition of kinases such as Src and mTOR. The potential efficacy of tumor-targeted TNFalpha is discussed, as well as the importance of preclinical validation of new targets. To improve the success of future clinical trials, clinicians and basic researchers need to intensify their exchange. Finally, a case is made for individualized treatment of OS patients, based on interdisciplinary cooperation in dedicated Sarcoma Centers. Copyright © 2014 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Oncol Lett
                Oncol Lett
                OL
                Oncology Letters
                D.A. Spandidos
                1792-1074
                1792-1082
                March 2019
                25 January 2019
                25 January 2019
                : 17
                : 3
                : 3133-3140
                Affiliations
                Department of Orthopaedics, Jingzhou Central Hospital, Jingzhou, Hubei 434020, P.R. China
                Author notes
                Correspondence to: Dr Shunguang Chen, Department of Orthopaedics, Jingzhou Central Hospital, 60 Jingzhong Road, Jingzhou, Hubei 434020, P.R. China, E-mail: rbnzs97@ 123456163.com
                Article
                OL-0-0-9975
                10.3892/ol.2019.9975
                6396117
                78a24ff9-ae0e-4c93-8828-bfa405a08ec7
                Copyright: © Chen et al.

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs 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
                : 24 April 2018
                : 18 December 2018
                Categories
                Articles

                Oncology & Radiotherapy
                osteosarcoma,e2f-mediated cell proliferation enhancing long non-coding rna,migration,rho-associated coiled-coil containing protein kinase 1,invasion

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