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- W4362495249 abstract "<div>Abstract<p>Small molecule inhibitors of AKT (v-akt murine thymoma viral oncogene homolog) signaling are being evaluated in patients with various cancer types, but have so far proven therapeutically disappointing for reasons that remain unclear. Here, we treat cancer cells with subtherapeutic doses of Akti-1/2, an allosteric small molecule AKT inhibitor, in order to experimentally model pharmacologic inhibition of AKT signaling <i>in vitro</i>. We then apply a combined RNA, protein, and metabolite profiling approach to develop an integrated, multiscale, molecular snapshot of this “AKT<sup>low</sup>” cancer cell state. We find that AKT-inhibited cancer cells suppress thousands of mRNA transcripts, and proteins related to the cell cycle, ribosome, and protein translation. Surprisingly, however, these AKT-inhibited cells simultaneously upregulate a host of other proteins and metabolites posttranscriptionally, reflecting activation of their endo-vesiculo-membrane system, secretion of inflammatory proteins, and elaboration of extracellular microvesicles. Importantly, these microvesicles enable rapidly proliferating cancer cells of various types to better withstand different stress conditions, including serum deprivation, hypoxia, or cytotoxic chemotherapy <i>in vitro</i> and xenografting <i>in vivo</i>. These findings suggest a model whereby cancer cells experiencing a partial inhibition of AKT signaling may actually promote the survival of neighbors through non-cell autonomous communication. <i>Mol Cancer Ther; 15(1); 142–53. ©2015 AACR</i>.</p></div>" @default.
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- W4362495249 date "2023-04-03" @default.
- W4362495249 modified "2023-09-28" @default.
- W4362495249 title "Data from AKT Inhibition Promotes Nonautonomous Cancer Cell Survival" @default.
- W4362495249 doi "https://doi.org/10.1158/1535-7163.c.6537610.v1" @default.
- W4362495249 hasPublicationYear "2023" @default.
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