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D‐dopachrome tautomerase promotes [beta]‐catenin‐dependent Cox‐2 expression in colorectal carcinoma.
Author(s) -
Xin Dan,
Zhao Ming,
Rendon Beatriz E,
Mitchell Robert A
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a108
Subject(s) - wnt signaling pathway , macrophage migration inhibitory factor , cancer research , signal transduction , beta catenin , cytokine , transcription factor , biology , colorectal cancer , cell growth , catenin , microbiology and biotechnology , immunology , cancer , genetics , gene
The small cytokine/growth factor, migration inhibitory factor(MIF) has recently been found to be a central participant in pro‐growth and metastatic tumor processes. To date, there is only one other known MIF family member, D‐dopachrome tautomerase(D‐DT). Among the many transcriptional targets that we have identified for MIF, one of the most intriguing is the Wnt signaling pathway component,[beta]‐catenin. We now have evidence that suggests that D‐DT functions in a similar manner as MIF and may in fact synergize to enhance MIF’s pro‐tumorigenic functions. Because [beta]‐catenin/TCF‐mediated transcription reportedly plays a central role in the development and maintenance of nearly all colorectal carcinomas(CRC), we sought to determine whether D‐DT could influence Wnt signaling in CRC. We now report that forced change of D‐DT in CRC cell lines effects [beta]‐catenin nuclear translocation accompanied by a significant change in cyclooxygenase‐2(Cox‐2) expression. Our studies reveal a novel regulatory role for this new cytokine/growth factor in Wnt signal transduction and the malignant phenotype(s) it promotes.