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ASN Neuro. 2018 Jan-Dec;10:1759091418781949. doi: 10.1177/1759091418781949.

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

Author information

1
1 Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Henan, P.R. China.
2
2 School of Life Sciences, Zhengzhou University, Henan, P.R. China.
3
3 Department of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, Henan, P.R. China.

Abstract

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.

KEYWORDS:

CLEC18B; Wnt/β-catenin; glioblastoma; migration; prognosis; proliferation

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