PMC

High level of CLEC18B predicted shorter overall survival (OS) in GBM patients. (a) Kaplan–Meier curves for OS according to CLEC18B expression in patients with GBM collected from TCGA. (b) Kaplan–Meier curves for OS according to CLEC18B expression in GBM patients collected at our institution.
CLEC18B = C-type lectin domain family 18 member B; GBM = glioblastoma multiforme; TCGA = The Cancer Genome Atlas.

The Wnt/β-catenin signaling was suppressed by knockdown of CLEC18B. (a) The key markers of Wnt/β-catenin signaling were measured by Western blot assay. (b) Box–whisker plot presenting the difference in protein levels in si-CLEC18B and si-NC groups. All values are shown as mean ± SD, **p  < .01 versus si-NC group. Assays were repeated three times.
CLEC18B = C-type lectin domain family 18 member B; si-NC = small interfering negative control; SD = standard deviation.

Migration and invasion capabilities of U87 and U251 cells were prohibited by CLEC18B knockdown. (a) The mobility of U87 cells was measured by wound-healing assay. (b) The migration and invasion of U87 cells were tested by transwell assay. (c) The mobility of U251 cells was measured by wound-healing assay. (d) The migration and invasion of U251 cells were tested by transwell assay. All values are shown as mean ± SD, **p  < .01 versus si-NC group. Assays were repeated three times.
CLEC18B = C-type lectin domain family 18 member B; si-NC = small interfering negative control; SD = standard deviation.

Elevated expression level of CLEC18B was observed in GBM tissues and cells. (a) Box plots of The Cancer Genome Atlas (TCGA) RNA expression analysis for CLEC18B. (b) Box plots of Oncomine datasets RNA expression analysis for CLEC18B. (c) RNA expression level of CLEC18B in clinical samples. (d) RNA expression level of CLEC18B in GBM cells and normal brain glial cell lines, HEB. All values are shown as mean ± SD, **p  < .01 versus normal, noncancerous tissues (ANT) or normal brain glial cell lines, HEB. Assays were repeated three times.
CLEC18B = C-type lectin domain family 18 member B; GBM = glioblastoma multiforme; HEB = human normal brain glial cell lines; ANT = adjacent noncancerous tissues; SD = standard deviation.

Growth and colony-formation abilities of GBM cells were inhibited by CLEC18B knockdown. (a to c) Transfection efficacy of CLEC18B si-RNA in U87 and U251 cells was analyzed by qPCR and Western blot assay, respectively. (d) Assessing the effects of CLEC18B downregulation on the proliferation ability of U87 and U251 cells using CCK-8 assay. (e) Evaluating the effects of CLEC18B knockdown on the colony-formation ability of U87 and U251 cells. All values are shown as mean ± SD, **p  < .01 versus si-NC group. Assays were repeated three times.
CLEC18B = C-type lectin domain family 18 member B; GBM = glioblastoma multiforme; si-RNA = small interfering RNA; qPCR = quantitative polymerase chain reaction; CCK-8 = Cell Counting Kit-8; si-NC = small interfering negative control; GAPDH = glyceraldehyde 3-phosphate dehydrogenase; SD = standard deviation.