"Taken together, these results suggest that activated Ki-Ras-mediated signals are involved in the SEK1-JNK pathway through a PKC isotype that is distinct from that involved in MEK1/2-ERK activation in human colon cancer cells and independent of phosphoinositol 3-kinase activation, and the imbalance between ERK and JNK activity caused by activated Ki-Ras may play critical roles in human colorectal tumorigenesis."
"JNK was originally identified as a kinase activated by H-Ras [XREF_BIBR, XREF_BIBR], but subsequently, it was demonstrated that mutated K-Ras activates JNK in vitro and in vivo [XREF_BIBR, XREF_BIBR]."
"Together, our findings suggest that pancreatic CSCs/CSLCs are dependent on K-Ras activation of JNK and also suggest that the K-Ras - JNK axis could be a potential target in CSC/CSLC-directed therapies against pancreatic cancer."
"The significance of JNK activation in pancreatic cancer biology remained unclear, but we have only recently demonstrated that JNK activation by KRas, which is mutationally activated in the majority of pancreatic cancers, plays a key role in the maintenance of self-renewal and tumor initiating capacity of pancreatic CSCs [XREF_BIBR]."
"Both the ERK and p38 MAPK pathways, but not JNK, were activated by KRAS (G12V) and we observed that proliferation and CAFC formation were mediated via ERK, while differentiation was predominantly mediated via p38."
"Unexpectedly, in tumors induced by the K12D oncogene, the K-Ras mutant protein does not interact with Raf-1 nor activates the Erk canonical pathway. Instead, it transduces signals through the PI3K/Akt, JNK, p38 and FAK pathways."