The tyrosine phosphorylated pro-survival form of Fas intensifies the EGF-induced signal in colorectal cancer cells through the nuclear EGFR/STAT3-mediated pathway.

In any case, the new information we presented regarding opposing roles of two closely related and ubiquitous SFKs in the activation of an emerging drug target such as STAT3 in the pathway of a major clinical drug target like EGFR is highly significant, particularly in consideration of the alternative or combinatory application of SFK inhibitors in anti-cancer therapies.

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