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Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition
Long non-coding RNAs (lncRNAs) have been demonstrated to serve vital roles in renal cell carcinoma (RCC) development. Gastric carcinoma high expressed transcript 1 (GHET1) regulates numerous biological processes in cancer cells. However, the biological role of GHET1 in RCC has not yet been identifie...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396227/ https://www.ncbi.nlm.nih.gov/pubmed/30867747 http://dx.doi.org/10.3892/ol.2019.9967 |
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author | Xie, Wenjie Liu, Xin Chen, Qiang Ma, Ming Yang, Xiaorong Gong, Binbin Sun, Ting Chen, Jie |
author_facet | Xie, Wenjie Liu, Xin Chen, Qiang Ma, Ming Yang, Xiaorong Gong, Binbin Sun, Ting Chen, Jie |
author_sort | Xie, Wenjie |
collection | PubMed |
description | Long non-coding RNAs (lncRNAs) have been demonstrated to serve vital roles in renal cell carcinoma (RCC) development. Gastric carcinoma high expressed transcript 1 (GHET1) regulates numerous biological processes in cancer cells. However, the biological role of GHET1 in RCC has not yet been identified. This study aimed to investigate the role of GHET1 in RCC. In the present study, the expression of GHET1 in RCC tissues and the 786-O, A498 and 293 cell lines was assessed by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, colony formation and cell scratch assays were used to determine the effects of GHET1 on tumorigenesis. Western blotting was performed to examine the effect of GHET1 on epithelial-mesenchymal transition (EMT) in RCC cells. GHET1 expression was significantly increased in the RCC samples in comparison with adjacent tissues. High expression levels of GHET1 were associated with distant metastasis and clinical stage severity, thus, high GHET1 expression may serve as a predictor for a poor prognosis. In addition, RCC cells presented higher GHET1 mRNA and protein expression levels compared with in 293 cells. Furthermore, silencing GHET1 suppressed cell growth, weakened cell migration and inhibited EMT of RCC cells in vitro. In conclusion, the present study suggested that GHET1 may be considered a therapeutic target for the treatment or prevention of RCC. |
format | Online Article Text |
id | pubmed-6396227 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-63962272019-03-13 Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition Xie, Wenjie Liu, Xin Chen, Qiang Ma, Ming Yang, Xiaorong Gong, Binbin Sun, Ting Chen, Jie Oncol Lett Articles Long non-coding RNAs (lncRNAs) have been demonstrated to serve vital roles in renal cell carcinoma (RCC) development. Gastric carcinoma high expressed transcript 1 (GHET1) regulates numerous biological processes in cancer cells. However, the biological role of GHET1 in RCC has not yet been identified. This study aimed to investigate the role of GHET1 in RCC. In the present study, the expression of GHET1 in RCC tissues and the 786-O, A498 and 293 cell lines was assessed by reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8, colony formation and cell scratch assays were used to determine the effects of GHET1 on tumorigenesis. Western blotting was performed to examine the effect of GHET1 on epithelial-mesenchymal transition (EMT) in RCC cells. GHET1 expression was significantly increased in the RCC samples in comparison with adjacent tissues. High expression levels of GHET1 were associated with distant metastasis and clinical stage severity, thus, high GHET1 expression may serve as a predictor for a poor prognosis. In addition, RCC cells presented higher GHET1 mRNA and protein expression levels compared with in 293 cells. Furthermore, silencing GHET1 suppressed cell growth, weakened cell migration and inhibited EMT of RCC cells in vitro. In conclusion, the present study suggested that GHET1 may be considered a therapeutic target for the treatment or prevention of RCC. D.A. Spandidos 2019-03 2019-01-25 /pmc/articles/PMC6396227/ /pubmed/30867747 http://dx.doi.org/10.3892/ol.2019.9967 Text en Copyright: © Xie 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 Xie, Wenjie Liu, Xin Chen, Qiang Ma, Ming Yang, Xiaorong Gong, Binbin Sun, Ting Chen, Jie Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
title | Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
title_full | Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
title_fullStr | Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
title_full_unstemmed | Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
title_short | Silencing of the long non-coding RNA GHET1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
title_sort | silencing of the long non-coding rna ghet1 inhibits cell proliferation and migration of renal cell carcinoma through epithelial-mesenchymal transition |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396227/ https://www.ncbi.nlm.nih.gov/pubmed/30867747 http://dx.doi.org/10.3892/ol.2019.9967 |
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