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LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma
INTRODUCTION: Ribosomal protein SA pseudogene 52 (RPSAP52) has been characterized as an oncogenic lncRNA in pituitary tumors. Analysis of TCGA dataset revealed the upregulation of RPSAP52 in glioblastoma (GBM). We, therefore, investigated the roles of RPSAP52 in GBM. METHODS: A total of 50 GBM patie...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170709/ https://www.ncbi.nlm.nih.gov/pubmed/32368136 http://dx.doi.org/10.2147/CMAR.S227496 |
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author | Wang, Shuwei Guo, Xinru Lv, Wenying Li, Yanteng Zhang, Leiming Dong, Chao Zhang, Jianning Cheng, Gang |
author_facet | Wang, Shuwei Guo, Xinru Lv, Wenying Li, Yanteng Zhang, Leiming Dong, Chao Zhang, Jianning Cheng, Gang |
author_sort | Wang, Shuwei |
collection | PubMed |
description | INTRODUCTION: Ribosomal protein SA pseudogene 52 (RPSAP52) has been characterized as an oncogenic lncRNA in pituitary tumors. Analysis of TCGA dataset revealed the upregulation of RPSAP52 in glioblastoma (GBM). We, therefore, investigated the roles of RPSAP52 in GBM. METHODS: A total of 50 GBM patients (33 males and 20 females; 54–75 years; mean age: 61.8±5.8 years) were selected from the 89 cases of GBM patients. Under the guidance of MRI, brain biopsy was performed to collect GBM tissues from each patient for the diagnosis of GBM. U-373 MG cells were employed and had transient transfections. qRNA, Western blot, and a series of experiments were performed to characterize their associations. RESULTS: The results showed that RPSAP52 was upregulated in GBM patients, and its high expression levels predicted poor survival. In GBM tissues, expression levels of RPSAP52 were significantly and positively correlated with that of TGF-β1. In GBM tissues, RPSAP52 positively regulated the expression of TGF-β1. Cell stemness assay showed that, compared to C and NC groups, overexpression of RPSAP52 and TGF-β1 led to increased, while silencing of RPSAP52 led to decreased CD133+ cells. Overexpression of TGF-β1 attenuated the effects of RPSAP52 siRNA silencing. CONCLUSION: Therefore, RPSAP52 upregulates TGF-β1 to increase cancer cell stemness and predict postoperative survival in GBM. |
format | Online Article Text |
id | pubmed-7170709 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-71707092020-05-04 LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma Wang, Shuwei Guo, Xinru Lv, Wenying Li, Yanteng Zhang, Leiming Dong, Chao Zhang, Jianning Cheng, Gang Cancer Manag Res Original Research INTRODUCTION: Ribosomal protein SA pseudogene 52 (RPSAP52) has been characterized as an oncogenic lncRNA in pituitary tumors. Analysis of TCGA dataset revealed the upregulation of RPSAP52 in glioblastoma (GBM). We, therefore, investigated the roles of RPSAP52 in GBM. METHODS: A total of 50 GBM patients (33 males and 20 females; 54–75 years; mean age: 61.8±5.8 years) were selected from the 89 cases of GBM patients. Under the guidance of MRI, brain biopsy was performed to collect GBM tissues from each patient for the diagnosis of GBM. U-373 MG cells were employed and had transient transfections. qRNA, Western blot, and a series of experiments were performed to characterize their associations. RESULTS: The results showed that RPSAP52 was upregulated in GBM patients, and its high expression levels predicted poor survival. In GBM tissues, expression levels of RPSAP52 were significantly and positively correlated with that of TGF-β1. In GBM tissues, RPSAP52 positively regulated the expression of TGF-β1. Cell stemness assay showed that, compared to C and NC groups, overexpression of RPSAP52 and TGF-β1 led to increased, while silencing of RPSAP52 led to decreased CD133+ cells. Overexpression of TGF-β1 attenuated the effects of RPSAP52 siRNA silencing. CONCLUSION: Therefore, RPSAP52 upregulates TGF-β1 to increase cancer cell stemness and predict postoperative survival in GBM. Dove 2020-04-15 /pmc/articles/PMC7170709/ /pubmed/32368136 http://dx.doi.org/10.2147/CMAR.S227496 Text en © 2020 Wang et al. http://creativecommons.org/licenses/by-nc/3.0/ 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). |
spellingShingle | Original Research Wang, Shuwei Guo, Xinru Lv, Wenying Li, Yanteng Zhang, Leiming Dong, Chao Zhang, Jianning Cheng, Gang LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma |
title | LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma |
title_full | LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma |
title_fullStr | LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma |
title_full_unstemmed | LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma |
title_short | LncRNA RPSAP52 Upregulates TGF-β1 to Increase Cancer Cell Stemness and Predict Postoperative Survival in Glioblastoma |
title_sort | lncrna rpsap52 upregulates tgf-β1 to increase cancer cell stemness and predict postoperative survival in glioblastoma |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7170709/ https://www.ncbi.nlm.nih.gov/pubmed/32368136 http://dx.doi.org/10.2147/CMAR.S227496 |
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