ArticleOncogene2007
Pharmacological inhibition of protein kinase CK2 reverts the multidrug resistance phenotype of a CEM cell line characterized by high CK2 level.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 90 citations in OpenAlex.
- Article
- CK2 in the spotlight: decoding its role in hematological malignancies and therapeutic applications.Discover oncology · 2025Review
- Regulation of cancer progression by CK2: an emerging therapeutic target.Medical oncology (Northwood, London, England) · 2024Review
- Inhibition of casein kinase 2 induces cell death in tyrosine kinase inhibitor resistant chronic myelogenous leukemia cells.PloS one · 2023Article
- A fragment-based approach leading to the discovery of inhibitors of CK2α with a novel mechanism of action.RSC medicinal chemistry · 2022Article
- Targeting CK2 in cancer: a valuable strategy or a waste of time?Cell death discovery · 2021Review
- Protein kinase CK2: a potential therapeutic target for diverse human diseases.Signal transduction and targeted therapy · 2021Review
- Article
- Quinalizarin, a specific CK2 inhibitor, can reduce icotinib resistance in human lung adenocarcinoma cell lines.International journal of molecular medicine · 2019Article
- Role of protein kinase CK2 in antitumor drug resistance.Journal of experimental & clinical cancer research : CR · 2019Review
- Inhibition of Casein Kinase 2 Disrupts Differentiation of Myeloid Cells in Cancer and Enhances the Efficacy of Immunotherapy in Mice.Cancer research · 2018Article
- Second-generation CK2α inhibitors targeting the αD pocket.Chemical science · 2018Article
- Therapeutic targeting of CK2 in acute and chronic leukemias.Leukemia · 2018Review
- Nuclear localization of the CK2α-subunit correlates with poor prognosis in clear cell renal cell carcinoma.Oncotarget · 2017Article
- Specific inhibition of CK2α from an anchor outside the active site.Chemical science · 2016Article
- Protein Kinase CK2α Maintains Extracellular Signal-regulated Kinase (ERK) Activity in a CK2α Kinase-independent Manner to Promote Resistance to Inhibitors of RAF and MEK but Not ERK in BRAF Mutant Melanoma.The Journal of biological chemistry · 2016Article
- Predicting CK2 beta-dependent substrates using linear patterns.Biochemistry and biophysics reports · 2015Article
- Protein kinase CK2 in breast cancer: the CK2β regulatory subunit takes center stage in epithelial plasticity.Cellular and molecular life sciences : CMLS · 2015Review
- Article
- Cell-permeable dual inhibitors of protein kinases CK2 and PIM-1: structural features and pharmacological potential.Cellular and molecular life sciences : CMLS · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein kinase CK2 is an ubiquitous and constitutively active kinase, which phosphorylates many cellular proteins and is implicated in the regulation of cell survival, proliferation and transformation. We investigated its possible involvement in the multidrug resistance phenotype (MDR) by analysing its level in two variants of CEM cells, namely S-CEM and R-CEM, normally sensitive or resistant to chemical apoptosis, respectively. We found that, while the CK2 regulatory subunit beta was equally expressed in the two cell variants, CK2alpha catalytic subunit was higher in R-CEM and this was accompanied by a higher phosphorylation of endogenous protein substrates. Pharmacological downregulation of CK2 activity by a panel of specific inhibitors, or knockdown of CK2alpha expression by RNA interference, were able to induce cell death in R-CEM. CK2 inhibitors could promote an increased uptake of chemotherapeutic drugs inside the cells and sensitize them to drug-induced apoptosis in a co-operative manner. CK2 blockade was also effective in inducing cell death of a different MDR line (U2OS). We therefore conclude that inhibition of CK2 can be considered as a promising tool to revert the MDR phenotype.
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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.