IndraLab

Statements

KRAS activates JNK. 11 / 13
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"KRAS expression led to activation of JNK in pancreatic cancer cell lines."
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"In addition, oncogenic K-ras expression led to activation of JNK in pancreatic cancer cell lines."
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"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]."
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"In addition, although Rac1 is an attractive candidate molecule linking K-Ras and JNK [XREF_BIBR], it still remains to be delineated in this study how K-Ras activates JNK in CSLCs."
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"Notably, oncogenic K-Ras activated all MAPKs (JNK, ERK and p38); however, only p38 was involved in p47 (phox)-NOX1-dependent ROS generation and consequent transformation."
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"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."
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"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."
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"The altered conformational bias may clarify their distinct rates of GTP hydrolysis, nucleotide exchange, and phospholipid selectivity, as well as the different favored effectors; K-Ras interacts with Raf-1 and signals through MAPK and Ral guanine nucleotide dissociation stimulator (RalGDS), whereas K-Ras activates PI3K, c-Jun N-terminal kinase (JNK), p38, and focal adhesion kinase (FAK) pathways (110,111)."
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"For example, p38 and JNK can be activated by KRAS signaling and these kinases are more specific for ETS1 than ERG."
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"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]."
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"Combined, these data suggest that K-Ras activation of JNK has a critical role in the maintenance of the self-renewal and tumor initiating capacity of pancreatic CSCs and CSLCs."
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