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lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p
Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the lo...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7640367/ https://www.ncbi.nlm.nih.gov/pubmed/33125151 http://dx.doi.org/10.3892/or.2020.7821 |
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author | Mu, Yulong Tang, Qiang Feng, Haiyan Zhu, Luwen Wang, Yan |
author_facet | Mu, Yulong Tang, Qiang Feng, Haiyan Zhu, Luwen Wang, Yan |
author_sort | Mu, Yulong |
collection | PubMed |
description | Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the long non-coding RNA (lncRNA) Kinectin 1-Antisense RNA 1 (KTN1-AS1) can participate in the development of several types of cancer. However, the underlying mechanism of KTN1-AS1 in GBM remains unknown. The present study aimed to determine the potential role of KTN1-AS1 in GBM. In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1-AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Furthermore, KTN1-AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo. In addition, high level of KTN1-AS1 was correlated with poor prognosis in TCGA GBM database. Furthermore, microRNA-505-3p (miR-505-3p) was a promising target of KTN1-AS1, and the suppressing effects of miR-505-3p on cell proliferation and invasive ability was reversed by downregulating KTN1-AS1. Taken together, the results from the present provided novel insights into the roles of KTN1-AS1 in GBM, and suggested that the KTN1-AS1/miR-505-3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM. |
format | Online Article Text |
id | pubmed-7640367 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-76403672020-11-04 lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p Mu, Yulong Tang, Qiang Feng, Haiyan Zhu, Luwen Wang, Yan Oncol Rep Articles Glioblastoma (GBM) is one of the most prevalent and aggressive central nervous tumors with high mobility and mortality. The prognosis of patients with GBM is poor. It is therefore essential to explore the therapeutic strategies for the treatment of GBM. Previous studies have demonstrated that the long non-coding RNA (lncRNA) Kinectin 1-Antisense RNA 1 (KTN1-AS1) can participate in the development of several types of cancer. However, the underlying mechanism of KTN1-AS1 in GBM remains unknown. The present study aimed to determine the potential role of KTN1-AS1 in GBM. In this study, reverse transcription quantitative PCR analysis was conducted and the results demonstrated that KTN1-AS1 was upregulated in GBM tissues and cell lines compared with normal tissues and astrocytes (NHA). Furthermore, KTN1-AS1 knockdown decreased the viability and invasive ability of glioma cells in vitro and in vivo. In addition, high level of KTN1-AS1 was correlated with poor prognosis in TCGA GBM database. Furthermore, microRNA-505-3p (miR-505-3p) was a promising target of KTN1-AS1, and the suppressing effects of miR-505-3p on cell proliferation and invasive ability was reversed by downregulating KTN1-AS1. Taken together, the results from the present provided novel insights into the roles of KTN1-AS1 in GBM, and suggested that the KTN1-AS1/miR-505-3p axis may be considered as a novel therapeutic target for the treatment of patients with GBM. D.A. Spandidos 2020-12 2020-10-22 /pmc/articles/PMC7640367/ /pubmed/33125151 http://dx.doi.org/10.3892/or.2020.7821 Text en Copyright: © Mu et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , 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. |
spellingShingle | Articles Mu, Yulong Tang, Qiang Feng, Haiyan Zhu, Luwen Wang, Yan lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p |
title | lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p |
title_full | lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p |
title_fullStr | lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p |
title_full_unstemmed | lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p |
title_short | lncRNA KTN1-AS1 promotes glioma cell proliferation and invasion by negatively regulating miR-505-3p |
title_sort | lncrna ktn1-as1 promotes glioma cell proliferation and invasion by negatively regulating mir-505-3p |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7640367/ https://www.ncbi.nlm.nih.gov/pubmed/33125151 http://dx.doi.org/10.3892/or.2020.7821 |
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