TY - JOUR
T1 - Wnt signaling stimulates transcriptional outcome of the hedgehog pathway by stabilizing GLI1 mRNA
AU - Noubissi, Felicite K.
AU - Goswami, Srikanta
AU - Sanek, Nicholas A.
AU - Kawakami, Kazuyuki
AU - Minamoto, Toshinari
AU - Moser, Amy
AU - Grinblat, Yevgenya
AU - Spiegelman, Vladimir S.
PY - 2009/11/15
Y1 - 2009/11/15
N2 - Wnt and Hedgehog signaling pathways play central roles in embryogenesis, stem cell maintenance, and tumorigenesis. However, the mechanisms by which these two pathways interact are not well understood. Here, we identified a novel mechanism by which Wnt signaling pathway stimulates the transcriptional output of Hedgehog signaling. Wnt/β-catenin signaling induces expression of an RNA-binding protein, CRD-BP, which in turn binds and stabilizes GLI1 mRNA, causing an elevation of GLI1 expression and transcriptional activity. The newly described mode of regulation of GLI1 seems to be important to several functions of Wnt, including survival and proliferation of colorectal cancer cells.
AB - Wnt and Hedgehog signaling pathways play central roles in embryogenesis, stem cell maintenance, and tumorigenesis. However, the mechanisms by which these two pathways interact are not well understood. Here, we identified a novel mechanism by which Wnt signaling pathway stimulates the transcriptional output of Hedgehog signaling. Wnt/β-catenin signaling induces expression of an RNA-binding protein, CRD-BP, which in turn binds and stabilizes GLI1 mRNA, causing an elevation of GLI1 expression and transcriptional activity. The newly described mode of regulation of GLI1 seems to be important to several functions of Wnt, including survival and proliferation of colorectal cancer cells.
UR - http://www.scopus.com/inward/record.url?scp=72249119222&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=72249119222&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-09-1500
DO - 10.1158/0008-5472.CAN-09-1500
M3 - Article
C2 - 19887615
AN - SCOPUS:72249119222
SN - 0008-5472
VL - 69
SP - 8572
EP - 8578
JO - Cancer Research
JF - Cancer Research
IS - 22
ER -