Cancer stem cell drugs target K-ras signaling in a stemness context.

This K-ras-specific activity of salinomycin may be significant, as the overexpression of H-rasG12V negatively regulates K-ras nanoclustering via segregation of PS. 18 Thus, H-rasG12V nanoclustering antagonizes an increase in K-ras nanoclustering and signaling.

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This was further supported by correlating the drug response profiles with the gene expression signature, which confirmed that the salinomycin response showed a positive trend of association with KRAS expression, but negative in particular with the expression of caveolar genes (Cav-1, Cav-2, PTRF) ( Figure 5e ).

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