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Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma
BACKGROUND: CELSR2 is postulated to be a receptor involved in contact-mediated communication; however, the specific function of this particular member has not been determined in hepatocellular carcinoma (HCC). METHODS: Here, we explored the expression and function of CELSR2 in HCC patients through d...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161135/ https://www.ncbi.nlm.nih.gov/pubmed/32293343 http://dx.doi.org/10.1186/s12885-020-06813-5 |
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author | Xu, Mingxing Zhu, Shu Xu, Ruiyun Lin, Nan |
author_facet | Xu, Mingxing Zhu, Shu Xu, Ruiyun Lin, Nan |
author_sort | Xu, Mingxing |
collection | PubMed |
description | BACKGROUND: CELSR2 is postulated to be a receptor involved in contact-mediated communication; however, the specific function of this particular member has not been determined in hepatocellular carcinoma (HCC). METHODS: Here, we explored the expression and function of CELSR2 in HCC patients through data mining and examined the results using clinical samples and in vitro experiments. RESULTS: It was found that CELSR2 mRNA and protein expression levels were significantly higher in cancerous tissue than in normal tissue. The increased mRNA expression of CELSR2 was significantly associated with overall survival (OS) in HCC patients. Moreover, the genetic alteration rate of CELSR2 gene in HCC can reach 8%, and these alterations would deeply influence its neighboring genes, then jointly affecting the occurrence and development of tumor through cell adhesion and numerous common carcinogenic pathways. Our in vitro results indicated that the depletion of CELSR2 inhibited liver cancer cell proliferation and invasion. Univariate and multivariate Cox regression analyses showed that CELSR2 could be viewed as an independent risk factor for HCC patients. CONCLUSIONS: This study demonstrated that data mining could efficiently reveal the roles of CELSR2 in HCC and its potential regulatory networks. The CELSR2 protein level may serve as a novel prognostic biomarker for HCC. |
format | Online Article Text |
id | pubmed-7161135 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-71611352020-04-22 Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma Xu, Mingxing Zhu, Shu Xu, Ruiyun Lin, Nan BMC Cancer Research Article BACKGROUND: CELSR2 is postulated to be a receptor involved in contact-mediated communication; however, the specific function of this particular member has not been determined in hepatocellular carcinoma (HCC). METHODS: Here, we explored the expression and function of CELSR2 in HCC patients through data mining and examined the results using clinical samples and in vitro experiments. RESULTS: It was found that CELSR2 mRNA and protein expression levels were significantly higher in cancerous tissue than in normal tissue. The increased mRNA expression of CELSR2 was significantly associated with overall survival (OS) in HCC patients. Moreover, the genetic alteration rate of CELSR2 gene in HCC can reach 8%, and these alterations would deeply influence its neighboring genes, then jointly affecting the occurrence and development of tumor through cell adhesion and numerous common carcinogenic pathways. Our in vitro results indicated that the depletion of CELSR2 inhibited liver cancer cell proliferation and invasion. Univariate and multivariate Cox regression analyses showed that CELSR2 could be viewed as an independent risk factor for HCC patients. CONCLUSIONS: This study demonstrated that data mining could efficiently reveal the roles of CELSR2 in HCC and its potential regulatory networks. The CELSR2 protein level may serve as a novel prognostic biomarker for HCC. BioMed Central 2020-04-15 /pmc/articles/PMC7161135/ /pubmed/32293343 http://dx.doi.org/10.1186/s12885-020-06813-5 Text en © The Author(s) 2020 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Article Xu, Mingxing Zhu, Shu Xu, Ruiyun Lin, Nan Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma |
title | Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma |
title_full | Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma |
title_fullStr | Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma |
title_full_unstemmed | Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma |
title_short | Identification of CELSR2 as a novel prognostic biomarker for hepatocellular carcinoma |
title_sort | identification of celsr2 as a novel prognostic biomarker for hepatocellular carcinoma |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7161135/ https://www.ncbi.nlm.nih.gov/pubmed/32293343 http://dx.doi.org/10.1186/s12885-020-06813-5 |
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