ReviewFrontiers in oncology2020
Protein Kinase CK2 in Cancer Energetics.
Review in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- CK2 in triple-negative breast cancer: oncogenic signaling networks and emerging CK2 inhibitor-based combination therapies.Clinical and experimental medicine · 2026Review
- Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis.Brain : a journal of neurology · 2026Article
- Comparative Efficacy of CK2 Inhibitors CX-4945 and SGC-CK2-2 on CK2 Signaling.International journal of molecular sciences · 2025Article
- Advances in pyrazolo[1,5-RSC advances · 2025Review
- Polyamines protect porcine sperm from lipopolysaccharide-induced mitochondrial dysfunction and apoptosis via casein kinase 2 activation.Journal of animal science · 2025Article
- Sanqi oral solution alleviates podocyte apoptosis in experimental membranous nephropathy by mediating EMT through the ERK/CK2-α/β-catenin pathway.Frontiers in pharmacology · 2025Article
- CK2 activity is crucial for proper glucagon expression.Diabetologia · 2024Article
- DYRK1A signalling synchronizes the mitochondrial import pathways for metabolic rewiring.Nature communications · 2024Article
- Cancer selective cell death induction by a bivalent CK2 inhibitor targeting the ATP site and the allosteric αD pocket.iScience · 2024Article
- Formulation and Investigation of CK2 Inhibitor-Loaded Alginate Microbeads with Different Excipients.Pharmaceutics · 2023Article
- CSNK2B modulates IRF1 binding to functional DNA elements and promotes basal and agonist-induced antiviral signaling.Nucleic acids research · 2023Article
- CircNDST1 promotes papillary thyroid cancer progression via its interaction with CSNK2A1 to activate the PI3K-Akt pathway and epithelial-mesenchymal transition.Journal of endocrinological investigation · 2023Article
- Analysis of the phosphoproteome of CK2Open biology · 2023Article
- Article
- CK2-Mediated Phosphorylation Upregulates the Stability of USP13 and Promotes Ovarian Cancer Cell Proliferation.Cancers · 2022Article
- Protein Kinase CK2 Controls CD8Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- CK2 Inhibition and Antitumor Activity of 4,7-Dihydro-6-nitroazolo[1,5-a]pyrimidines.Molecules (Basel, Switzerland) · 2022Article
- CK2 and the Hallmarks of Cancer.Biomedicines · 2022Review
- The Role of Protein Kinase CK2 in Development and Disease Progression: A Critical Review.Journal of developmental biology · 2022Review
- Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase CK2 (formerly known as casein kinase 2) is abnormally elevated in many cancers. This may increase tumor aggressiveness through CK2-dependent phosphorylation of key proteins in several signaling pathways. In this work, we have compiled evidence from the literature to suggest that CK2 also modulates a metabolic switch characteristic of cancer cells that enhances resistance to death, due to either drugs or to a microenvironment deficient in oxygen or nutrients. Concurrently, CK2 may help to preserve mitochondrial activity in a PTEN-dependent manner. PTEN, widely recognized as a tumor suppressor, is another CK2 substrate in the PI3K/Akt signaling pathway that promotes cancer viability and aerobic glycolysis. Given that CK2 can regulate Akt as well as two of its main effectors, namely mTORC1 and β-catenin, we comprehensively describe how CK2 may modulate cancer energetics by regulating expression of key targets and downstream processes, such as HIF-1 and autophagy, respectively. Thus, the specific inhibition of CK2 may lead to a catastrophic death of cancer cells, which could become a feasible therapeutic strategy to beat this devastating disease. In fact, ATP-competitive inhibitors, synthetic peptides and antisense oligonucleotides have been designed as CK2 inhibitors, some of them used in preclinical models of cancer, of which TBB and silmitasertib are widely known. We will finish by discussing a hypothetical scenario in which cancer cells are "addicted" to CK2; i.e., in which many proteins that regulate signaling pathways and metabolism-linked processes are highly dependent on this kinase.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.