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Updated: Feb 2, 2026
Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
Published on: May 3, 2018
Coupling function of cyclin-dependent kinase 2 and Septin2 in the promotion of hepatocellular carcinoma
Chenzhou Xu1,2, Wei Zhang1,2, Xuening Zhang1,2
1Department of Gastroenterology, Affiliated Hospital of Nantong University, Nantong, China.
Abstract:
Hepatocellular carcinoma (HCC) is a common and aggressive malignant tumor with a poorly defined molecular mechanism. Cyclin-dependent kinase 2 (CDK2) and Septin2 (SEPT2) are 2 known oncogenic molecules but the mechanism of functional interactions remains unclear. Here, we interestingly found that CDK2 and SEPT2 show very similar dynamic expression during the cell cycle. Both CDK2 and SEPT2 show the highest protein levels in the G2/M phase, resulting in CDK2 interacting with SEPT2 and stabilizing SEPT2 in HCC. In a panel of 8 pairs of fresh HCC tissues and corresponding adjacent tissues, both western blot and immunohistochemistry (IHC) assays demonstrate that CDK2 expression is highly correlated with SEPT2. HCC with high expression of both CDK2 and SEPT2 are more likely to relapse. This observation is further demonstrated by a large panel of 100 HCC patients. In this large panel, high expression of both CDK2 and SEPT2 significantly correlates with tumor differentiation and microvascular invasion, which is an independent prognostic factor in HCC patients. In summary, our results reveal a cooperative function between CDK2 and SEPT2. HCC with high expression of CDK2 and SEPT2 might be more aggressive and respond poorly to current therapy.
Insights
Hepatocellular carcinoma (HCC) involves Cyclin-dependent kinase 2 (CDK2) and Septin2 (SEPT2) interacting and stabilizing each other. High expression of both CDK2 and SEPT2 correlates with aggressive HCC and poor prognosis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Hepatocellular carcinoma (HCC) is a prevalent and aggressive malignancy with incompletely understood molecular drivers.
- Cyclin-dependent kinase 2 (CDK2) and Septin2 (SEPT2) are recognized oncogenic molecules, but their functional interplay in HCC is unclear.
Purpose of the Study:
- To investigate the interaction and functional relationship between CDK2 and SEPT2 in Hepatocellular Carcinoma.
- To determine the clinical significance of CDK2 and SEPT2 co-expression in HCC patient outcomes.
Main Methods:
- Western blot and immunohistochemistry (IHC) assays were performed on HCC tissues and adjacent non-tumorous tissues.
- Analysis included 8 paired fresh HCC tissues and a larger cohort of 100 HCC patients.
Main Results:
- CDK2 and SEPT2 exhibit similar dynamic expression patterns, peaking in the G2/M phase.
- CDK2 interacts with and stabilizes SEPT2 in HCC cells.
- High co-expression of CDK2 and SEPT2 correlates significantly with tumor differentiation, microvascular invasion, and increased likelihood of relapse in HCC patients.
Conclusions:
- CDK2 and SEPT2 exhibit a cooperative oncogenic function in HCC.
- Elevated CDK2 and SEPT2 expression indicates a more aggressive HCC phenotype and potentially poorer response to therapy.
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