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Hedgehog signaling is activated in canine transitional cell carcinoma and contributes to cell proliferation and survival
Author(s) -
Gustafson T. L.,
Kitchell B. E.,
Biller B.
Publication year - 2017
Publication title -
veterinary and comparative oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 34
eISSN - 1476-5829
pISSN - 1476-5810
DOI - 10.1111/vco.12149
Subject(s) - cyclopamine , hedgehog , transitional cell carcinoma , hedgehog signaling pathway , cancer research , cell growth , apoptosis , urinary bladder , signal transduction , cell culture , urothelial cell , biology , carcinoma , chemistry , pathology , medicine , microbiology and biotechnology , urothelium , cancer , bladder cancer , biochemistry , genetics
Transitional cell carcinoma (TCC) is the most commonly diagnosed tumor of the canine urinary system. Hedgehog (HH) signaling represents one possible novel therapeutic target, based on its recently identified central role in human urothelial carcinoma. The purpose of this study was to determine if HH mediators are expressed in canine TCC and the effect of inhibition of this pathway on cell growth and survival. HH pathway mediators were found to be expressed in five canine TCC cell lines. Indian HH was expressed in tumor cells in five canine bladder tumor tissues, but not in normal canine bladder tissue. Inhibition of HH signaling with cyclopamine and GANT61 led to significantly decreased cell proliferation but had a smaller effect on apoptosis. These results support future investigation of inhibitors of HH signaling in the treatment of canine TCC.

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