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- W2279386089 abstract "A177 Transcriptional changes in response to hypoxia are regulated in part through MAP kinase signaling to AP-1, and thus contribute to resistance of cancer cells to therapy, including platinum compounds. A key role for JNK in this signaling is supported by pharmacological inhibitor studies in our previous work. In this study of the up-stream mediators of hypoxic signaling to AP-1/c-Jun in the HT29 colon adenocarcinoma cell line, we have observed significant activation of stress-activated pathways mediated by SEK1 and MKK7, with lesser or no changes in pathways regulated by constitutive active MEK3/6 and MEK1/2. Introduction of dominant negative MKK7 exerted a greater inhibitory effect on AP-1 binding activity during hypoxia than that of SEK1. Experiments with HT29-derived cell lines stably expressing mutant SEK1 or MKK7 (HTS13 and HTM9, respectively) demonstrated a requirement for functional MKK7 for activation of the JNK/c-Jun cascade, and hypoxic activation of the AP-1 transcription factor. Inhibition of MKK7 also led to a significant increase in oxaliplatin resistance under hypoxia/reoxygenation, as demonstrated in MTT and colony-forming assays, whereas inhibition of SEK1 rendered cells more sensitive under these circumstances. Finally, HTM9-derived tumors were resistant to oxaliplatin alone, to bevacizumab, and to the combination of oxaliplatin and bevacizumab in a mouse xenograft model. Our data support a positive contribution of MKK7/JNK to oxaliplatin cytotoxicity, and identify SEK1 as a potential target for reversal of hypoxic resistance to oxaliplatin." @default.
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- W2279386089 date "2007-11-01" @default.
- W2279386089 modified "2023-09-28" @default.
- W2279386089 title "Signaling through MKK7 is required for oxaliplatin-induced cell death in hypoxic colon adenocarcinoma cell lines" @default.
- W2279386089 hasPublicationYear "2007" @default.
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