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• W2148691917 endingPage "331" @default.
• W2148691917 startingPage "331" @default.
• W2148691917 abstract "In rapidly growing tumors, hypoxia commonly develops due to the imbalance between O2 consumption and supply. Hypoxia Inducible Factor (HIF)-1α is a transcription factor responsible for tumor growth and angiogenesis in the hypoxic microenvironment; thus, its inhibition is regarded as a promising strategy for cancer therapy. Given that CamKII or PARP inhibitors are emerging anticancer agents, we investigated if they have the potential to be developed as new HIF-1α-targeting drugs. When treating various cancer cells with the inhibitors, we found that a CamKII inhibitor, KN-62, effectively suppressed HIF-1α specifically in hepatoma cells. To examine the effect of KN-62 on HIF-1α-driven gene expression, we analyzed the EPO-enhancer reporter activity and mRNA levels of HIF-1α downstream genes, such as EPO, LOX and CA9. Both the reporter activity and the mRNA expression were repressed by KN-62. We also found that KN-62 suppressed HIF-1α by impairing synthesis of HIF-1α protein. Based on these results, we propose that KN-62 is a candidate as a HIF-1α-targeting anticancer agent." @default.
• W2148691917 created "2016-06-24" @default.
• W2148691917 creator A5006080567 @default.
• W2148691917 date "2010-01-01" @default.
• W2148691917 modified "2023-10-16" @default.
• W2148691917 title "CaMKII Inhibitor KN-62 Blunts Tumor Response to Hypoxia by Inhibiting HIF-1α in Hepatoma Cells" @default.
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• W2148691917 doi "https://doi.org/10.4196/kjpp.2010.14.5.331" @default.
• W2148691917 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2997420" @default.
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• W2148691917 hasPublicationYear "2010" @default.
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