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CDK9: A Comprehensive Review of Its Biology, and Its Role as a Potential Target for Anti-Cancer Agents

Abel Tesfaye Anshabo1, Robert Milne1, Shudong Wang1

  • 1Drug Discovery and Development, Centre for Cancer Diagnostics and Therapeutics, Clinical and Health Sciences, University of South Australia, Adelaide, SA, Australia.

Frontiers in Oncology
|May 27, 2021
PubMed

Insights

Cyclin-dependent kinases (CDKs) regulate cell division and transcription. Dysregulated CDK9 is crucial in cancer, driving tumor survival and making CDK9 inhibitors a promising therapeutic strategy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Cyclin-dependent kinases (CDKs) are critical regulators of cellular processes, including cell division and transcription.
  • Dysregulation of CDKs is a significant factor in cancer development and progression.
  • Transcriptional CDKs, particularly CDK9, play a vital role in maintaining cancer cell survival by regulating gene expression.

Purpose of the Study:

  • To provide a comprehensive overview of CDK9 structure and biology.
  • To elucidate the role of CDK9 in both solid and hematological malignancies.
  • To review current CDK9 inhibitors in preclinical and clinical development.

Main Methods:

  • Literature review of CDK9 structure, function, and involvement in cancer.
  • Analysis of preclinical and clinical data on CDK9 inhibitors.
  • Synthesis of information on CDK9 pathway dysregulation in various cancers.

Main Results:

  • CDK9 is a key regulator of transcription essential for cancer cell survival.
  • CDK9 pathway dysregulation is evident across diverse hematological and solid tumors.
  • Several CDK9 inhibitors have demonstrated therapeutic potential and advanced to clinical trials.

Conclusions:

  • CDK9 represents a significant therapeutic target for cancer treatment.
  • Targeting CDK9 offers a promising strategy for combating various malignancies.
  • Ongoing research and clinical trials are evaluating the efficacy of CDK9 inhibitors.
Keywords:
CDK9 inhibitorsCDKsP-TEFbcancertranscription

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