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Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma

C-type lectin domain family 18 member B (CLEC18B), encoding a superfamily of CLEC, has been found to be expressed in some of cancer cells, which possibly indicates it associated with cancer. However, the defined functional characterizations of CLEC18B in glioblastoma multiforme (GBM) progression sti...

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Autores principales: Guo, Rui-Ming, Zhao, Cheng-Bin, Li, Peng, Zhang, Liang, Zang, Su-Hua, Yang, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024345/
https://www.ncbi.nlm.nih.gov/pubmed/29914265
http://dx.doi.org/10.1177/1759091418781949
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author Guo, Rui-Ming
Zhao, Cheng-Bin
Li, Peng
Zhang, Liang
Zang, Su-Hua
Yang, Bo
author_facet Guo, Rui-Ming
Zhao, Cheng-Bin
Li, Peng
Zhang, Liang
Zang, Su-Hua
Yang, Bo
author_sort Guo, Rui-Ming
collection PubMed
description C-type lectin domain family 18 member B (CLEC18B), encoding a superfamily of CLEC, has been found to be expressed in some of cancer cells, which possibly indicates it associated with cancer. However, the defined functional characterizations of CLEC18B in glioblastoma multiforme (GBM) progression still remain unclear. To this end, clinical relevance of CLEC18B expression with GBM patients’ prognosis was analyzed both in The Cancer Genome Atlas dataset of 174 tissues and 40 GBM tumor tissues collected from our hospital by using the Kaplan–Meier survival and the Cox proportional hazard model. The role of CLEC18B in GBM was determined by loss-of-function assay using small interfering RNA approach in vitro. Functional and signaling analyses were also performed to understand how CLEC18B facilitated the aggressiveness of GBM at molecular and cellular levels using Cell Counting Kit-8 assay, wound-healing, transwell, and Western blot analyses. Results from our analyses showed that CLEC18B was markedly elevated in both GBM tissues and cells, and exhibited strong inverse correlation with overall survival in GBM patients. Moreover, CLEC18B was identified as an independent predictor of patient survival. Functionally, knockdown of CLEC18B inhibited the growth, migration, and invasion of GBM cells. Mechanistic studies revealed that silencing of CLEC18B resulted in downregulation of Wnt/β-catenin signaling activity. Collectively, our findings provide clinical, molecular, and cellular evidence of CLEC18B as a promising prognostic biomarker and therapeutic target for GBM.
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spelling pubmed-60243452018-07-05 Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma Guo, Rui-Ming Zhao, Cheng-Bin Li, Peng Zhang, Liang Zang, Su-Hua Yang, Bo ASN Neuro Original Paper C-type lectin domain family 18 member B (CLEC18B), encoding a superfamily of CLEC, has been found to be expressed in some of cancer cells, which possibly indicates it associated with cancer. However, the defined functional characterizations of CLEC18B in glioblastoma multiforme (GBM) progression still remain unclear. To this end, clinical relevance of CLEC18B expression with GBM patients’ prognosis was analyzed both in The Cancer Genome Atlas dataset of 174 tissues and 40 GBM tumor tissues collected from our hospital by using the Kaplan–Meier survival and the Cox proportional hazard model. The role of CLEC18B in GBM was determined by loss-of-function assay using small interfering RNA approach in vitro. Functional and signaling analyses were also performed to understand how CLEC18B facilitated the aggressiveness of GBM at molecular and cellular levels using Cell Counting Kit-8 assay, wound-healing, transwell, and Western blot analyses. Results from our analyses showed that CLEC18B was markedly elevated in both GBM tissues and cells, and exhibited strong inverse correlation with overall survival in GBM patients. Moreover, CLEC18B was identified as an independent predictor of patient survival. Functionally, knockdown of CLEC18B inhibited the growth, migration, and invasion of GBM cells. Mechanistic studies revealed that silencing of CLEC18B resulted in downregulation of Wnt/β-catenin signaling activity. Collectively, our findings provide clinical, molecular, and cellular evidence of CLEC18B as a promising prognostic biomarker and therapeutic target for GBM. SAGE Publications 2018-06-18 /pmc/articles/PMC6024345/ /pubmed/29914265 http://dx.doi.org/10.1177/1759091418781949 Text en © The Author(s) 2018 http://creativecommons.org/licenses/by-nc/4.0/ Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Paper
Guo, Rui-Ming
Zhao, Cheng-Bin
Li, Peng
Zhang, Liang
Zang, Su-Hua
Yang, Bo
Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma
title Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma
title_full Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma
title_fullStr Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma
title_full_unstemmed Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma
title_short Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma
title_sort overexpression of clec18b associates with the proliferation, migration, and prognosis of glioblastoma
topic Original Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024345/
https://www.ncbi.nlm.nih.gov/pubmed/29914265
http://dx.doi.org/10.1177/1759091418781949
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