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Updated: Feb 9, 2026

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
Published on: May 3, 2018
Cyclin‑dependent kinase 10 prevents glioma metastasis via modulation of Snail expression
Hui Li1, Yanjie You2, Jianfeng Liu1
1Department of Neurosurgery, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, P.R. China.
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.
Insights
Cyclin-dependent kinase 10 (CDK10) acts as a tumor suppressor in glioma. Downregulation of CDK10 promotes glioma cell metastasis by activating Snail-driven epithelial-mesenchymal transition (EMT), suggesting CDK10 as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cyclin-dependent kinase 10 (CDK10) is implicated as a tumor suppressor in various cancers.
- The role of CDK10 in glioma biology and regulation remains largely unexplored.
Purpose of the Study:
- To investigate the biological and regulatory functions of CDK10 in glioma.
- To determine the association between CDK10 expression and glioma cell proliferation, metastasis, and epithelial-mesenchymal transition (EMT).
Main Methods:
- Overexpression and knockdown of CDK10 in glioma cell lines.
- Assessment of cell proliferation and metastasis.
- Analysis of epithelial-mesenchymal transition (EMT) markers and Snail (SNAI1) expression.
Main Results:
- CDK10 overexpression inhibited glioma cell proliferation and metastasis.
- CDK10 knockdown promoted glioma cell proliferation and metastasis.
- Downregulated CDK10 expression correlated with epithelial-mesenchymal transition (EMT) and increased Snail expression.
- Silencing Snail expression reversed EMT phenotypes induced by CDK10 knockdown.
Conclusions:
- CDK10 downregulation promotes glioma metastasis through Snail-driven EMT.
- CDK10 functions as a tumor suppressor in glioma.
- CDK10 represents a potential molecular target for glioma therapy.
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