Coupling function of CDK2 and SEPT2 in the promotion of hepatocellular carcinoma

Abstract

Hepatocellular carcinoma (HCC) is a common and aggressive malignant tumor with poorly defined molecular mechanism. Cyclin‐dependent kinase 2 (CDK2) and Septin2 (SEPT2) are two 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 cell cycle. Both CDK2 and SEPT2 show highest protein level in G2/M phase, resulting in the fact that CDK2 interacts with SEPT2 and stabilizes SEPT2 in HCCs. In a panel of eight pairs of fresh HCC tissues and corresponding adjacent tissues, both WB and IHC assays demonstrate that CDK2 expression is highly correlated with SEPT2. HCCs 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 such 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. HCCs with high expression of CDK2 and SEPT2 might be more aggressive and response poorly to current therapy.

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