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Published on: October 4, 2019
CKAP2L Knockdown Exerts Antitumor Effects by Increasing miR-4496 in Glioblastoma Cell Lines
Yao-Feng Li1, Wen-Chiuan Tsai1, Chung-Hsing Chou2,3
1Department of Pathology, Tri-Service General Hospital, National Defense Medical Center, Taipei 11490, Taiwan.
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.
Insights
Cytoskeleton-associated protein 2-like (CKAP2L) promotes glioma progression by regulating cell division and migration. Inhibiting CKAP2L may offer a new therapeutic strategy for glioma patients, impacting survival rates.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Genetics
Background:
- Glioma, a central nervous system malignancy, has poor patient survival despite treatment advances.
- Cytoskeleton-associated protein 2-like (CKAP2L) is implicated in neural progenitor cell division and lung cancer prognosis.
Purpose of the Study:
- To investigate the role of CKAP2L in glioma development and progression.
- To explore CKAP2L as a potential prognostic marker for glioma.
Main Methods:
- Bioinformatics analysis of The Cancer Gene Atlas and Chinese Glioma Genome Atlas datasets.
- Gene Set Enrichment Analysis (GSEA) to identify enriched phenotypes.
- In vitro experiments using human glioma cell lines (U87MG, U118MG, LNZ308) with CKAP2L knockdown (siCKAP2L).
- Analysis of cell proliferation, migration, invasion, epithelial-mesenchymal transition, cell cycle, and microRNA expression (miR-4496).
Main Results:
- CKAP2L expression correlates with glioma tumor grade and patient overall survival.
- High CKAP2L expression is associated with enriched phenotypes like mitotic spindle and G2/M checkpoint.
- CKAP2L knockdown inhibits glioma cell proliferation, migration, invasion, and EMT, inducing G2/M cell cycle arrest.
- CKAP2L knockdown increases miR-4496 levels, and manipulating miR-4496 mimics or reverses CKAP2L knockdown effects.
Conclusions:
- CKAP2L is a crucial regulator of glioma cell proliferation, migration, and cell cycle progression.
- CKAP2L acts as a regulator of miR-4496 activity in glioma.
- CKAP2L represents a potential prognostic biomarker and therapeutic target for glioma.
