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• W2068305148 abstract "Transforming growth factor activated kinase 1 (TAK1) provides prosurvival signals in various types of cells, and emerging evidence indicates that targeting TAK1 is a promising means to eliminate certain types of cancer cells. Here, we show that TAK1 is required for efficient tumorigenicity of AKT-transformed cells. TAK1 inhibition accelerates cell apoptosis of AKT-transformed cells in anchorage-independent cell growth accompanying by the downregulation of Mcl-1 and Bcl-2 expression. On the contrary, the tumorigenicity of c-Myc-transformed cells is not significantly affected by TAK1 inhibition. Moreover, AKT-transformed cells with c-Myc overexpression tolerate TAK1 inhibition in anchorage-independent growth and tumorigenicity in vivo. Together, our results provide evidence that TAK1-dependency in the tumorigenicity of AKT-transformed cells can be alleviated by c-Myc overexpression. These findings suggest that dual-targeting TAK1 and c-Myc might be a rational therapeutic strategy for treatment of certain types of cancer." @default.
• W2068305148 created "2016-06-24" @default.
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• W2068305148 date "2013-08-01" @default.
• W2068305148 modified "2023-09-27" @default.
• W2068305148 title "c-MYC overexpression overrides TAK1 dependency in efficient tumorigenicity of AKT-transformed cells" @default.
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• W2068305148 doi "https://doi.org/10.1016/j.canlet.2013.03.014" @default.
• W2068305148 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23523871" @default.
• W2068305148 hasPublicationYear "2013" @default.
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