TY - JOUR
T1 - Wnt signaling in cancer
T2 - Not a binary on:off switch
AU - Flanagan, Dustin J.
AU - Vincan, Elizabeth
AU - Phesse, Toby J.
N1 - Funding Information:
Funding is gratefully acknowledged from the following: National Health and Medical Research Council of Australia (NHMRC, 566679, and APP1099302 to E. Vincan and T.J. Phesse), Melbourne Health project grants (605030 and PG-002 to E. Vincan and T.J. Phesse), Medical Research Council (MR/R026424/1 to T.J. Phesse), Early Career Researcher grant (GIA-033 to D.J. Flanagan), Cancer Council of Victoria project grants (CCV, APP1020716 to E. Vincan and T.J. Phesse), CCV Fellowship (to D.J. Flanagan), and Cardiff University/CMU Research Fellowship (to T.J. Phesse).
Publisher Copyright:
© 2019 American Association for Cancer Research.
PY - 2019/12
Y1 - 2019/12
N2 - In the March 1 issue of Cancer Research, we identified the Wnt receptor Fzd7 as an attractive therapeutic target for the treatment of gastric cancer. In summary, we showed that pharmacological inhibition of Wnt receptors, or genetic deletion of Fzd7, blocks the initiation and growth of gastric tumors. Inhibiting Fzd receptors, specifically Fzd7, inhibits the growth of gastric cancer cells even in the presence of adenomatous polyposis coli (Apc) mutation. Apc is located in the cytoplasm downstream of Fzd7 in the Wnt signaling cascade and APC mutations activate Wnt/b-catenin signaling, therefore, this result seems counterintuitive. Here, we analyze this result in greater detail in the context of current knowledge of Wnt signaling and discuss the wider implications of this aspect of Wnt signaling in other cancers.
AB - In the March 1 issue of Cancer Research, we identified the Wnt receptor Fzd7 as an attractive therapeutic target for the treatment of gastric cancer. In summary, we showed that pharmacological inhibition of Wnt receptors, or genetic deletion of Fzd7, blocks the initiation and growth of gastric tumors. Inhibiting Fzd receptors, specifically Fzd7, inhibits the growth of gastric cancer cells even in the presence of adenomatous polyposis coli (Apc) mutation. Apc is located in the cytoplasm downstream of Fzd7 in the Wnt signaling cascade and APC mutations activate Wnt/b-catenin signaling, therefore, this result seems counterintuitive. Here, we analyze this result in greater detail in the context of current knowledge of Wnt signaling and discuss the wider implications of this aspect of Wnt signaling in other cancers.
UR - http://www.scopus.com/inward/record.url?scp=85075961720&partnerID=8YFLogxK
U2 - 10.1158/0008-5472.CAN-19-1362
DO - 10.1158/0008-5472.CAN-19-1362
M3 - Review Article
C2 - 31431458
AN - SCOPUS:85075961720
SN - 0008-5472
VL - 79
SP - 5901
EP - 5906
JO - Cancer Research
JF - Cancer Research
IS - 23
ER -
