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Updated: Oct 13, 2025

Identification of Novel CK2 Kinase Substrates Using a Versatile Biochemical Approach
Published on: February 21, 2019
CSNK2 in cancer: pathophysiology and translational applications
Scott W Strum1, Laszlo Gyenis2, David W Litchfield3
1Department of Medicine, Western University, Schulich School of Medicine & Dentistry, London, ON, Canada. sstrum@uwo.ca.
Abstract:
Protein kinase CSNK2 (CK2) is a pleiotropic serine/threonine kinase frequently dysregulated in solid and hematologic malignancies. To consolidate a wide range of biological and clinically oriented data from this unique kinase in cancer, this systematic review summarises existing knowledge from in vitro, in vivo and pre-clinical studies on CSNK2 across 24 different human cancer types. CSNK2 mRNA transcripts, protein levels and activity were found to be routinely upregulated in cancer, and commonly identified phosphotargets included AKT, STAT3, RELA, PTEN and TP53. Phenotypically, it frequently influenced evasion of apoptosis, enhancement of proliferation, cell invasion/metastasis and cell cycle control. Clinically, it held prognostic significance across 14 different cancers, and its inhibition in xenograft experiments resulted in a positive treatment response in 12. In conjunction with commentary on preliminary studies of CSNK2 inhibitors in humans, this review harmonises an extensive body of CSNK2 data in cancer and reinforces its emergence as an attractive target for cancer therapy. Continuing to investigate CSNK2 will be crucial to advancing our understanding of CSNK2 biology, and offers the promise of important new discoveries scientifically and clinically.
Insights
Protein kinase CSNK2 (CK2) is frequently dysregulated in cancers. This review consolidates data showing CK2 upregulation and its role in cancer progression, supporting its potential as a therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Protein kinase CSNK2 (CK2) is a serine/threonine kinase implicated in various cellular processes.
- CK2 is frequently dysregulated in both solid and hematologic malignancies, suggesting a role in cancer development and progression.
Purpose of the Study:
- To systematically review and consolidate existing knowledge on CSNK2 in cancer.
- To evaluate the biological and clinical significance of CSNK2 across diverse human cancer types.
Main Methods:
- Systematic literature review of in vitro, in vivo, and preclinical studies.
- Analysis of CSNK2 expression, activity, phosphotargets, and phenotypic effects in 24 human cancer types.
- Evaluation of clinical prognostic significance and response to CSNK2 inhibition in preclinical models.
Main Results:
- CSNK2 mRNA, protein levels, and activity are routinely upregulated in cancer.
- Key phosphotargets include AKT, STAT3, RELA, PTEN, and TP53, influencing apoptosis evasion, proliferation, invasion, and cell cycle.
- CSNK2 has prognostic significance in 14 cancers, and its inhibition showed positive responses in 12 xenograft models.
Conclusions:
- CSNK2 is a consistently upregulated kinase in cancer, driving key oncogenic phenotypes.
- CSNK2 inhibition demonstrates preclinical efficacy, highlighting its potential as a cancer therapeutic target.
- Further investigation of CSNK2 is crucial for advancing cancer biology understanding and developing novel therapies.
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