Abstract
Despite advances in the diagnosis and treatment of the central nervous system malignancy glioma, overall survival remains poor. Cytoskeleton-associated protein 2-like (CKAP2L), which plays key roles in neural progenitor cell division, has also been linked to poor prognosis in lung cancer. In the present study, we investigated the role of CKAP2L in glioma. From bioinformatics analyses of datasets from The Cancer Gene Atlas and the Chinese Glioma Genome Atlas, we found that CKAP2L expression correlates with tumor grade and overall survival. Gene set enrichment analysis (GSEA) showed that MITOTIC_SPINDLE, G2M_CHECKPOINT, and E2F_TARGETS are crucially enriched phenotypes associated with high CKAP2L expression. Using U87MG, U118MG, and LNZ308 human glioma cells, we confirmed that CKAP2L knockdown with siCKAP2L inhibits glioma cell proliferation, migration, invasion, and epithelial-mesenchymal transition. Interestingly, CKAP2L knockdown also induced cell cycle arrest at G2/M phase, which is consistent with the GSEA finding. Finally, we observed that CKAP2L knockdown led to significant increases in miR-4496. Treating cells with exogenous miR-4496 mimicked the effect of CKAP2L knockdown, and the effects of CKAP2L knockdown could be suppressed by miR-4496 inhibition. These findings suggest that CKAP2L is a vital regulator of miR-4496 activity and that CKAP2L is a potentially useful prognostic marker in glioma.
Highlights
IntroductionCentral nervous system (CNS) malignancies are responsible for significant morbidity and mortality worldwide [1]
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.license.Central nervous system (CNS) malignancies are responsible for significant morbidity and mortality worldwide [1]
Among the 701 The Cancer Genome Atlas (TCGA) samples, we found that Cytoskeleton-associated protein 2-like (CKAP2L) expression correlated significantly (p < 0.0001) with tumor grade (Figure 1A)
Summary
Central nervous system (CNS) malignancies are responsible for significant morbidity and mortality worldwide [1]. Among CNS malignancies, glioma is the most common, accounting for 26% of all CNS neoplasms [2]. Before 2016, glioma diagnoses were based on cellular morphology and included astrocytoma, oligodendroglioma, and ependymoma, based on the 4th version of WHO Classification for Brain Tumors [4]. Since the revision of the 4th edition of the WHO Classification [3] and recent updates [5,6,7], the molecular information has played a critical role in prognosis prediction and treatment, such as IDH1/2 [8,9], 1p19q [3], EGFR amplification [6], combined whole chromosome
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