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Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer
INTRODUCTION: Ovarian cancer (OC) is one of the most common malignancies and the leading cause of cancer-related death among women. The long non-coding RNA Prostate cancer-associated transcript-1 (PCAT-1) has been reported to play important roles in multiple human cancers. However, the role of PCAT-...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Termedia Publishing House
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6425202/ https://www.ncbi.nlm.nih.gov/pubmed/30899305 http://dx.doi.org/10.5114/aoms.2018.75534 |
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author | Gu, Li-Ping Jin, Shuo Xu, Rong-Chun Zhang, Jing Geng, Ying-Chun Shao, Xing-Yue Qin, Li-Bo |
author_facet | Gu, Li-Ping Jin, Shuo Xu, Rong-Chun Zhang, Jing Geng, Ying-Chun Shao, Xing-Yue Qin, Li-Bo |
author_sort | Gu, Li-Ping |
collection | PubMed |
description | INTRODUCTION: Ovarian cancer (OC) is one of the most common malignancies and the leading cause of cancer-related death among women. The long non-coding RNA Prostate cancer-associated transcript-1 (PCAT-1) has been reported to play important roles in multiple human cancers. However, the role of PCAT-1 in OC has never been investigated. The purpose of this study was to investigate the expression and roles of PCAT-1 in OC. MATERIAL AND METHODS: Expression of PCAT-1 and miR-129-5p in OC tissues and cell lines was determined by qRT-PCR. Cell proliferation and apoptosis were analyzed by MTT assay and flow cytometry, respectively. The interaction between PCAT-1 and miR-129-5p was demonstrated by luciferase reporter assay. RESULTS: PCAT-1 is significantly upregulated in OC tissues and cell lines (p < 0.05). Overexpression of PCAT-1 promotes proliferation of OC cells and inhibits their apoptosis (p < 0.05). In addition, miR-129-5p is markedly downregulated in OC and its level is inversely correlated with PCAT-1 expression in OC tumor tissues (p < 0.05). miR-129-5p inhibits proliferation and induces apoptosis in OC cell lines (p < 0.05). Furthermore, it has been demonstrated that miR-129-5p is directly targeted by PCAT-1 and miR-129-5p overexpression can effectively attenuate the effects of PCAT-1 on the proliferation and apoptosis of OC cells. CONCLUSIONS: Our results suggest that PCAT-1 functions as an oncogene by inhibiting miR-129-5p in OC and silencing PCAT-1 may be a novel therapeutic strategy in the treatment of OC. |
format | Online Article Text |
id | pubmed-6425202 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Termedia Publishing House |
record_format | MEDLINE/PubMed |
spelling | pubmed-64252022019-03-21 Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer Gu, Li-Ping Jin, Shuo Xu, Rong-Chun Zhang, Jing Geng, Ying-Chun Shao, Xing-Yue Qin, Li-Bo Arch Med Sci Basic Research INTRODUCTION: Ovarian cancer (OC) is one of the most common malignancies and the leading cause of cancer-related death among women. The long non-coding RNA Prostate cancer-associated transcript-1 (PCAT-1) has been reported to play important roles in multiple human cancers. However, the role of PCAT-1 in OC has never been investigated. The purpose of this study was to investigate the expression and roles of PCAT-1 in OC. MATERIAL AND METHODS: Expression of PCAT-1 and miR-129-5p in OC tissues and cell lines was determined by qRT-PCR. Cell proliferation and apoptosis were analyzed by MTT assay and flow cytometry, respectively. The interaction between PCAT-1 and miR-129-5p was demonstrated by luciferase reporter assay. RESULTS: PCAT-1 is significantly upregulated in OC tissues and cell lines (p < 0.05). Overexpression of PCAT-1 promotes proliferation of OC cells and inhibits their apoptosis (p < 0.05). In addition, miR-129-5p is markedly downregulated in OC and its level is inversely correlated with PCAT-1 expression in OC tumor tissues (p < 0.05). miR-129-5p inhibits proliferation and induces apoptosis in OC cell lines (p < 0.05). Furthermore, it has been demonstrated that miR-129-5p is directly targeted by PCAT-1 and miR-129-5p overexpression can effectively attenuate the effects of PCAT-1 on the proliferation and apoptosis of OC cells. CONCLUSIONS: Our results suggest that PCAT-1 functions as an oncogene by inhibiting miR-129-5p in OC and silencing PCAT-1 may be a novel therapeutic strategy in the treatment of OC. Termedia Publishing House 2018-04-30 2019-03 /pmc/articles/PMC6425202/ /pubmed/30899305 http://dx.doi.org/10.5114/aoms.2018.75534 Text en Copyright: © 2018 Termedia & Banach http://creativecommons.org/licenses/by-nc-sa/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license. |
spellingShingle | Basic Research Gu, Li-Ping Jin, Shuo Xu, Rong-Chun Zhang, Jing Geng, Ying-Chun Shao, Xing-Yue Qin, Li-Bo Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer |
title | Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer |
title_full | Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer |
title_fullStr | Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer |
title_full_unstemmed | Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer |
title_short | Long non-coding RNA PCAT-1 promotes tumor progression by inhibiting miR-129-5p in human ovarian cancer |
title_sort | long non-coding rna pcat-1 promotes tumor progression by inhibiting mir-129-5p in human ovarian cancer |
topic | Basic Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6425202/ https://www.ncbi.nlm.nih.gov/pubmed/30899305 http://dx.doi.org/10.5114/aoms.2018.75534 |
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