ArticleMolecular and cellular biochemistry2017
Inhibition of protein kinase CK2 sensitizes non-small cell lung cancer cells to cisplatin via upregulation of PML.
Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Inhibition of protein kinase CK2 remodels the tumor immune microenvironment and sensitizes lung cancer to PD-L1 blockade.Experimental hematology & oncology · 2026Article
- Development, anti-proliferative activity, multi-target kinase inhibition against CHK1, PIM1, and CDK-2, and computational insights of new thiazole-based hybrids.RSC advances · 2026Article
- Cryo-EM structure of PML RBCC dimer reveals CC-mediated octopus-like nuclear body assembly mechanism.Cell discovery · 2024Article
- CIGB-300 internalizes and impairs viability of NSCLC cells lacking actionable targets by inhibiting casein kinase-2 signaling.Scientific reports · 2024Article
- Article
- Targeting CK2 in cancer: a valuable strategy or a waste of time?Cell death discovery · 2021Review
- CX-4945 and siRNA-Mediated Knockdown of CK2 Improves Cisplatin Response in HPV(+) and HPV(-) HNSCC Cell Lines.Biomedicines · 2021Article
- ALKBH5 Inhibited Cell Proliferation and Sensitized Bladder Cancer Cells to Cisplatin by m6A-CK2α-Mediated Glycolysis.Molecular therapy. Nucleic acids · 2021Article
- Coordinated targeting of CK2 and KIT in gastrointestinal stromal tumours.British journal of cancer · 2020Article
- Role of protein kinase CK2 in antitumor drug resistance.Journal of experimental & clinical cancer research : CR · 2019Review
- Identification of a Two-Gene (Frontiers in oncology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung carcinoma (NSCLC), a malignancy of lungs, is very aggressive and usually ends up with a dismal prognosis. Cisplatin (CDDP)-based systemic chemotherapy is the main pharmaceutical approach for treating NSCLC, but its effect is discounted by some hitherto unknown reasons. Thus, this study is dedicated to improving the efficacy of CDDP. Our results show that combining use of CDDP with CK2 siRNA or inhibitor is more efficient in suppressing cancer cell growth and promoting apoptosis than use of CDDP alone. The underlying mechanism is that CDDP has two pathways to go: one is that it directly induces apoptosis and the other is that it activates CK2, which suppresses proapoptosis gene promyelocytic leukemia (PML). In conclusion, inhibiting CK2 can enhance sensitivity of CDDP to NSCLC cancer cells through PML.
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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.