CDK8 is a member of the cyclin-dependent kinase family and is an integral component of the mediator complex, a multi-protein assembly that regulates transcription by RNA polymerase II. Unlike cell cycle CDKs, CDK8 primarily modulates transcriptional programs by phosphorylating transcription factors and other components of the transcription machinery. Its activity impacts various signaling pathways, including Wnt/β-catenin, Notch, and TGF-β, which are crucial for cell proliferation, differentiation, and survival.
Overexpression or hyperactivation of CDK8 has been reported in various cancers, including colorectal cancer, melanoma, breast cancer, and others. Such dysregulation can contribute to abnormal transcriptional programs that favor oncogenesis.
Elevated levels or increased activity of CDK8 can enhance oncogenic signaling pathways. For instance, its role in potentiating the Wnt/β-catenin pathway has been associated with tumor growth and progression in colorectal cancers.
High CDK8 expression or activity has frequently been linked to more aggressive tumor phenotypes. In several studies, increased CDK8 has correlated with advanced disease stages and features such as enhanced metastatic potential, increased cell proliferation, and resistance to certain therapies.
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