Cyclin‑dependent kinase 10 prevents glioma metastasis via modulation of Snail expression.

Abstract

Cyclin‑dependent kinase 10 (CDK10) has been indicated to be a candidate tumor suppressor in multiple cancer types. However, to the best of the authors' knowledge, its biological and regulatory functions in glioma have not been previously reported. In the present study, it was demonstrated that overexpression of CDK10 inhibited glioma cell proliferation and metastasis. By contrast, knockdown of CDK10 expression promoted these malignant phenotypes. It was additionally indicated that dysregulated CDK10 expression was associated with epithelial‑mesenchymal transition (EMT) and that it regulated the expression of zinc finger protein SNAI1 (Snail). Furthermore, silencing Snail expression rescued EMT phenotypes induced by CDK10 knockdown, suggesting that Snail may be involved in the mechanistic association between CDK10 and EMT. The present study illustrated that downregulation of CDK10 expression activated Snail‑driven EMT and consequently promoted glioma metastasis, suggesting that CDK10 may serve as a potential molecular target for glioma therapy.

• Authors: Hui Li, Yanjie You, Jianfeng Liu
• Journal: Molecular medicine reports (Mol Med Rep) Vol. 18 Issue 1 Pg. 1165-1170 (Jul 2018) ISSN: 1791-3004 [Electronic] Greece
• PMID: 29845196 (Publication Type: Journal Article)

Chemical References

• Neoplasm Proteins
• SNAI1 protein, human
• Snail Family Transcription Factors
• CDK10 protein, human
• Cyclin-Dependent Kinases

Topics

• Cell Line, Tumor
• Cyclin-Dependent Kinases (genetics, metabolism)
• Epithelial-Mesenchymal Transition
• Gene Expression Regulation, Neoplastic
• Glioma (genetics, metabolism, pathology)
• Humans
• Neoplasm Metastasis
• Neoplasm Proteins (genetics, metabolism)
• Snail Family Transcription Factors (biosynthesis, genetics)