Journal
CANCER CELL
Volume 11, Issue 5, Pages 447-460Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2007.03.009
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Funding
- NCI NIH HHS [R01 CA051995, R01 CA099961-03, R01 CA051995-15, R01 CA051995-14, R01 CA099961-04, CA 51995, R01 CA076098, R01 CA099961, CA 76098] Funding Source: Medline
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Constitutive activation of MEK-ERK signaling is often found in melanomas. Here, we identify a mechanism that links ERK with JNK signaling in human melanoma. Constitutively active ERK increases c-Jun transcription and stability, which are mediated by CREB and GSK3, respectively. Subsequently, c-Jun increases transcription of target genes, including RACK1, an adaptor protein that enables PKC to phosphorylate and enhance JNK activity, enforcing a feed-forward mechanism of the JNK-Jun pathway. Activated c-Jun is also responsible for elevated cyclin 131 expression, which is frequently overexpressed in human melanoma. Our data reveal that, in human melanoma, the rewired ERK signaling pathway upregulates JNK and activates the c-Jun oncogene and its downstream targets, including RACK1 and cyclin D1.
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