Unveiling the impact of CDK8 on tumor progression: mechanisms and therapeutic strategies

Xiaomin Yin; Zhilong He; Kun Chen; Kai Ouyang; Changxuan Yang; Jianjun Li; Hailin Tang; Manbo Cai

doi:10.3389/fphar.2024.1386929

Unveiling the impact of CDK8 on tumor progression: mechanisms and therapeutic strategies

Front Pharmacol. 2024 Mar 28:15:1386929. doi: 10.3389/fphar.2024.1386929. eCollection 2024.

Authors

Xiaomin Yin^#¹, Zhilong He^#¹, Kun Chen^#¹, Kai Ouyang¹, Changxuan Yang¹, Jianjun Li², Hailin Tang³, Manbo Cai¹

Affiliations

¹ 1 Department of Radiotherapy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
² Department of Urological Surgical, The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China.
³ State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China.

^# Contributed equally.

Abstract

CDK8 is an important member of the cyclin-dependent kinase family associated with transcription and acts as a key "molecular switch" in the Mediator complex. CDK8 regulates gene expression by phosphorylating transcription factors and can control the transcription process through Mediator complex. Previous studies confirmed that CDK8 is an important oncogenic factor, making it a potential tumor biomarker and a promising target for tumor therapy. However, CDK8 has also been confirmed to be a tumor suppressor, indicating that it not only promotes the development of tumors but may also be involved in tumor suppression. Therefore, the dual role of CDK8 in the process of tumor development is worth further exploration and summary. This comprehensive review delves into the intricate involvement of CDK8 in transcription-related processes, as well as its role in signaling pathways related to tumorigenesis, with a focus on its critical part in driving cancer progression.

Keywords: CDK8; DNA damage; cell cycle; energy metabolism; immune; invasion; tumorigenesis.

Publication types

Review

Grants and funding

The author(s) declare that financial support was received for the research, authorship, and/or publication of this article. The authors gratefully acknowledge financial support from the Natural Science Foundation of Hunan Province, China (2021JJ30610 and 2020JJ4539); and the Key Guiding Project of Hunan Provincial Health Commission (202104101985); the Science and Technology Innovation Project of Hengyang City (202150064015); the University of South China Teaching Reform Research Project (2020YB-XJG127).