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.

中文翻译：

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CLEC18B的过表达与胶质母细胞瘤的增殖，迁移和预后有关。

已经发现编码CLEC超家族的C型凝集素结构域家族18成员B（CLEC18B）在某些癌细胞中表达，这可能表明其与癌症有关。但是，CLEC18B在胶质母细胞瘤（GBM）进展中定义的功能表征仍不清楚。为此，我们采用Kaplan-Meier生存率和Cox比例风险模型，从我们医院收集的174个组织和40个GBM肿瘤组织的癌症基因组图集中分析了CLEC18B表达与GBM患者预后的临床相关性。CLEC18B在GBM中的作用是通过体外的小干扰RNA方法进行功能丧失测定来确定的。还进行了功能和信号分析，以了解CLEC18B如何使用Cell Counting Kit-8分析，伤口愈合，transwell和Western blot分析在分子和细胞水平上促进GBM的侵袭性。我们的分析结果表明，CLEC18B在GBM组织和细胞中均显着升高，并且与GBM患者的总生存率呈强反相关。此外，CLEC18B被确定为患者生存的独立预测指标。功能上，敲低CLEC18B抑制了GBM细胞的生长，迁移和侵袭。机理研究表明，CLEC18B沉默导致Wnt /β-catenin信号传导活性下调。总之，我们的发现提供了临床，分子，