http://www.cnr.it/ontology/cnr/individuo/prodotto/ID322673
Effects of the CK2 Inhibitors CX-4945 and CX-5011 on Drug-Resistant Cells (Articolo in rivista)
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- Effects of the CK2 Inhibitors CX-4945 and CX-5011 on Drug-Resistant Cells (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1371/journal.pone.0049193 (literal)
- Alternative label
Zanin, Sofia; Borgo, Christian; Girardi, Cristina; O'Brien, Sean E.; Miyata, Yoshihiko; Pinna, Lorenzo A.; Donella-Deana, Arianna; Ruzzene, Maria (2012)
Effects of the CK2 Inhibitors CX-4945 and CX-5011 on Drug-Resistant Cells
in PloS one
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Zanin, Sofia; Borgo, Christian; Girardi, Cristina; O'Brien, Sean E.; Miyata, Yoshihiko; Pinna, Lorenzo A.; Donella-Deana, Arianna; Ruzzene, Maria (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
- http://www.ncbi.nlm.nih.gov/pubmed/23145120 (literal)
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- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
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- ISI Web of Science (WOS) (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- 1 - 3, 7: Department of Biomedical Sciences and National Research Council Institute of Neurosciences, University of Padova, Padova, Italy;
4: Cylene Pharmaceuticals, San Diego,
California, United States of America;
5: Department of Cell and Developmental Biology, Graduate School of Biostudies, Kyoto University, Kyoto, Japan;
6, 8: Department of Biomedical Sciences and National Research Council Institute of Neurosciences, University of Padova, Padova, Italy / Venetian Institute
of Molecular Medicine, Padova, Italy (literal)
- Titolo
- Effects of the CK2 Inhibitors CX-4945 and CX-5011 on Drug-Resistant Cells (literal)
- Abstract
- CK2 is a pleiotropic protein kinase, which regulates many survival pathways and plays a global anti-apoptotic function. It is highly expressed in tumor cells, and is presently considered a promising therapeutic target. Among the many inhibitors available for this kinase, the recently developed CX-4945 and CX-5011 have proved to be very potent, selective and effective in inducing cell death in tumor cells; CX-4945 has recently entered clinical trials. However, no data are available on the efficacy of these compounds to overcome drug resistance, a major reasons of cancer therapy failure. Here we address this point, by studying their effects in several tumor cell lines, each available as variant R resistant to drug-induced apoptosis, and normal-sensitive variant S. We found that the inhibition of endogenous CK2 was very similar in S and R treated cells, with more than 50% CK2 activity reduction at sub-micromolar concentrations of CX-4945 and CX-5011. A consequent apoptotic response was induced both in S and R variants of each pairs. Moreover, the combined treatment of CX-4945 plus vinblastine was able to sensitize to vinblastine R cells that are otherwise almost insensitive to this conventional antitumor drug. Consistently, doxorubicin accumulation in multidrug resistant (MDR) cells was greatly increased by CX-4945. In summary, we demonstrated that all the R variants are sensitive to CX-4945 and CX-5011; since some of the treated R lines express the extrusion pump Pgp, often responsible of the MDR phenotype, we can also conclude that the two inhibitors can successfully overcome the MDR phenomenon. (literal)
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