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• W2131462105 endingPage "1976" @default.
• W2131462105 startingPage "1968" @default.
• W2131462105 abstract "The PI3K/PTEN/Akt/mTOR/p70S6K pathway is one of the most frequently deregulated signaling pathways in solid tumors and has a functional role in drug resistance. However, targeting this pathway leads to compensatory activation of several mediators of cell survival. Expression of the reactive oxygen species-controlling kinase Mirk/dyrk1B was increased severalfold by the mammalian target of rapamycin (mTOR) inhibitors RAD001, WYE354 and rapamycin, with less effect by the Akt inhibitors AZD5363 and MK-2206. Upregulation of Mirk messenger RNA (mRNA) expression was mediated by cyclic AMP response element binding protein (CREB) binding to two sites in the Mirk promoter upstream of the transcription start site and one site within exon 4. Depletion of CREB reduced Mirk expression, whereas depletion of mTOR increased it. Moreover, hydroxytamoxifen activation of an Akt-estrogen receptor construct blocked an increase in Mirk mRNA and protein. Addition of a Mirk/dyrk1B kinase inhibitor increased the sensitivity of Panc1 pancreatic cancer cells and three different ovarian cancer cell lines to the mTOR inhibitor RAD001. Targeting Mirk kinase could improve the utility of mTOR inhibitors and so presents an attractive drug target." @default.
• W2131462105 created "2016-06-24" @default.
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• W2131462105 date "2014-03-03" @default.
• W2131462105 modified "2023-10-16" @default.
• W2131462105 title "Mirk/dyrk1B kinase is upregulated following inhibition of mTOR" @default.
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• W2131462105 doi "https://doi.org/10.1093/carcin/bgu058" @default.
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