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Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells
Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcino...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031698/ https://www.ncbi.nlm.nih.gov/pubmed/29973643 http://dx.doi.org/10.1038/s41598-018-27837-9 |
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author | Sun, Han-Dong Xu, Zhi-Peng Sun, Zhi-Qiang Zhu, Bin Wang, Qian Zhou, Jian Jin, Hui Zhao, Andi Tang, Wei-Wei Cao, Xiu-Feng |
author_facet | Sun, Han-Dong Xu, Zhi-Peng Sun, Zhi-Qiang Zhu, Bin Wang, Qian Zhou, Jian Jin, Hui Zhao, Andi Tang, Wei-Wei Cao, Xiu-Feng |
author_sort | Sun, Han-Dong |
collection | PubMed |
description | Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcinogenesis. Human circRNA microarray was performed to screen for abnormally expressed circRNA in GC tissue. Results showed that a decrease in the circPVRL3 expression level was associated with the presence of GC, and also with higher TNM stage and lower overall survival rates compared with that in adjacent noncancerous tissues. In vitro assays of the GC cell lines MKN-45 and MGC-803 demonstrated that knockdown of circPVRL3 promoted cell proliferation significantly. Prediction and annotation revealed circPVRL3 was able to sponge to 9 miRNAs and may be also able to have a binding with AGO2, FUS, LIN28A, PTB, and EIF4A3. In addition, based on the structure of internal ribosomal entry sites, open reading frame, and m(6)A modification, circPVRL3 may have the potential ability to encode proteins. Taken together, our study indicated that down-regulation of circPVRL3 could promote the proliferation in gastric carcinoma and have potential to encode protein. |
format | Online Article Text |
id | pubmed-6031698 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-60316982018-07-12 Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells Sun, Han-Dong Xu, Zhi-Peng Sun, Zhi-Qiang Zhu, Bin Wang, Qian Zhou, Jian Jin, Hui Zhao, Andi Tang, Wei-Wei Cao, Xiu-Feng Sci Rep Article Circular RNA (circRNA) is a key regulator in the development and progression of various types of carcinomas. However, its role in gastric cancer (GC) tumorigenesis is not well understood. The present study aimed to investigate the expression profile and potential modulation of circRNAs on GC carcinogenesis. Human circRNA microarray was performed to screen for abnormally expressed circRNA in GC tissue. Results showed that a decrease in the circPVRL3 expression level was associated with the presence of GC, and also with higher TNM stage and lower overall survival rates compared with that in adjacent noncancerous tissues. In vitro assays of the GC cell lines MKN-45 and MGC-803 demonstrated that knockdown of circPVRL3 promoted cell proliferation significantly. Prediction and annotation revealed circPVRL3 was able to sponge to 9 miRNAs and may be also able to have a binding with AGO2, FUS, LIN28A, PTB, and EIF4A3. In addition, based on the structure of internal ribosomal entry sites, open reading frame, and m(6)A modification, circPVRL3 may have the potential ability to encode proteins. Taken together, our study indicated that down-regulation of circPVRL3 could promote the proliferation in gastric carcinoma and have potential to encode protein. Nature Publishing Group UK 2018-07-04 /pmc/articles/PMC6031698/ /pubmed/29973643 http://dx.doi.org/10.1038/s41598-018-27837-9 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Sun, Han-Dong Xu, Zhi-Peng Sun, Zhi-Qiang Zhu, Bin Wang, Qian Zhou, Jian Jin, Hui Zhao, Andi Tang, Wei-Wei Cao, Xiu-Feng Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
title | Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
title_full | Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
title_fullStr | Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
title_full_unstemmed | Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
title_short | Down-regulation of circPVRL3 promotes the proliferation and migration of gastric cancer cells |
title_sort | down-regulation of circpvrl3 promotes the proliferation and migration of gastric cancer cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6031698/ https://www.ncbi.nlm.nih.gov/pubmed/29973643 http://dx.doi.org/10.1038/s41598-018-27837-9 |
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