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Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195

A growing body of evidence has indicated that long non-coding RNAs (lncRNAs) serve as competing endogenous RNAs (ceRNAs) during oncogenesis. In this study, the qRT-PCR results indicated that the lncRNA PVT1 is overexpressed in osteosarcoma and decreased the survival rate of osteosarcoma patients. MT...

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Autores principales: Zhou, Quan, Chen, Fengli, Zhao, Jiali, Li, Baojun, Liang, Yong, Pan, Wei, Zhang, Shaoxian, Wang, Xinhong, Zheng, Donghui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5347719/
https://www.ncbi.nlm.nih.gov/pubmed/27813492
http://dx.doi.org/10.18632/oncotarget.13012
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author Zhou, Quan
Chen, Fengli
Zhao, Jiali
Li, Baojun
Liang, Yong
Pan, Wei
Zhang, Shaoxian
Wang, Xinhong
Zheng, Donghui
author_facet Zhou, Quan
Chen, Fengli
Zhao, Jiali
Li, Baojun
Liang, Yong
Pan, Wei
Zhang, Shaoxian
Wang, Xinhong
Zheng, Donghui
author_sort Zhou, Quan
collection PubMed
description A growing body of evidence has indicated that long non-coding RNAs (lncRNAs) serve as competing endogenous RNAs (ceRNAs) during oncogenesis. In this study, the qRT-PCR results indicated that the lncRNA PVT1 is overexpressed in osteosarcoma and decreased the survival rate of osteosarcoma patients. MTT and clonal colony formation assays were used to detect the effect of PVT1 on proliferation, and flow cytometry was performed to assess apoptosis and the cell cycle. A Transwell assay was used to analyze migration and invasion. The results revealed that silencing PVT1 by siRNA inhibited proliferation, migration and invasion and promoted apoptosis and cell cycle arrest in osteosarcoma cells. Furthermore, a gene microarray was used to screen differentially expressed miRNAs associated with PVT1. The interaction between PVT1 and miRNAs was then analyzed by qRT-PCR and luciferase reporter gene assay. We found that PVT1 negatively regulated miR-195 in osteosarcoma cells. Simultaneously, we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells. Moreover, silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1#1-induced apoptosis of U2OS cells. CCND1 inhibited the cell cycle arrest of U2OS cells induced by si-PVT1#1. FASN promoted the invasiveness U2OS cells, which was inhibited by si-PVT1#1. Therefore, our study demonstrated that PVT1 may be a therapeutic target for treatment of osteosarcoma.
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spelling pubmed-53477192017-03-31 Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195 Zhou, Quan Chen, Fengli Zhao, Jiali Li, Baojun Liang, Yong Pan, Wei Zhang, Shaoxian Wang, Xinhong Zheng, Donghui Oncotarget Research Paper A growing body of evidence has indicated that long non-coding RNAs (lncRNAs) serve as competing endogenous RNAs (ceRNAs) during oncogenesis. In this study, the qRT-PCR results indicated that the lncRNA PVT1 is overexpressed in osteosarcoma and decreased the survival rate of osteosarcoma patients. MTT and clonal colony formation assays were used to detect the effect of PVT1 on proliferation, and flow cytometry was performed to assess apoptosis and the cell cycle. A Transwell assay was used to analyze migration and invasion. The results revealed that silencing PVT1 by siRNA inhibited proliferation, migration and invasion and promoted apoptosis and cell cycle arrest in osteosarcoma cells. Furthermore, a gene microarray was used to screen differentially expressed miRNAs associated with PVT1. The interaction between PVT1 and miRNAs was then analyzed by qRT-PCR and luciferase reporter gene assay. We found that PVT1 negatively regulated miR-195 in osteosarcoma cells. Simultaneously, we found that silencing PVT1 by siRNA suppressed proliferation, migration and invasion and promoted cell cycle arrest and apoptosis via miR-195 in osteosarcoma cells. Moreover, silencing PVT1 by siRNA inhibited BCL2, CCND1, and FASN protein expression via miR-195 in osteosarcoma cells, and BCL2 inhibited the si-PVT1#1-induced apoptosis of U2OS cells. CCND1 inhibited the cell cycle arrest of U2OS cells induced by si-PVT1#1. FASN promoted the invasiveness U2OS cells, which was inhibited by si-PVT1#1. Therefore, our study demonstrated that PVT1 may be a therapeutic target for treatment of osteosarcoma. Impact Journals LLC 2016-11-02 /pmc/articles/PMC5347719/ /pubmed/27813492 http://dx.doi.org/10.18632/oncotarget.13012 Text en Copyright: © 2016 Zhou et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Zhou, Quan
Chen, Fengli
Zhao, Jiali
Li, Baojun
Liang, Yong
Pan, Wei
Zhang, Shaoxian
Wang, Xinhong
Zheng, Donghui
Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195
title Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195
title_full Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195
title_fullStr Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195
title_full_unstemmed Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195
title_short Long non-coding RNA PVT1 promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195
title_sort long non-coding rna pvt1 promotes osteosarcoma development by acting as a molecular sponge to regulate mir-195
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5347719/
https://www.ncbi.nlm.nih.gov/pubmed/27813492
http://dx.doi.org/10.18632/oncotarget.13012
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