The canine prostate cancer cell line CHP‐1 shows over‐expression of the co‐chaperone small glutamine‐rich tetratricopeptide repeat‐containing protein α

Although androgen therapy resistance and poor clinical outcomes are seen in most canine prostate cancer cases, there are only a few tools for analysing canine prostate cancer by using a cell biological approach. Therefore, to evaluate androgen‐independent neoplastic cell growth, a new canine prostat...

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Bibliographic Details
Published in:Veterinary & comparative oncology 2017-06, Vol.15 (2), p.557-562
Main Authors: Azakami, D., Nakahira, R., Kato, Y., Michishita, M., Kobayashi, M., Onozawa, E., Bonkobara, M., Takahashi, K., Watanabe, M., Ishioka, K., Sako, T., Ochiai, K., Omi, T.
Format: Article
Language:English
Subjects:
androgen receptor signalling
Animals
canine
Carrier Proteins - metabolism
Cell Line, Tumor
Dog Diseases - metabolism
Dog Diseases - pathology
Dogs
Glutamine
Male
Mice, Nude
Neoplasm Transplantation
Prostate - metabolism
Prostate - pathology
prostate cancer
Prostatic Neoplasms - metabolism
Prostatic Neoplasms - pathology
Prostatic Neoplasms - veterinary
Reverse Transcriptase Polymerase Chain Reaction - veterinary
small glutamine‐rich tetratricopeptide repeat‐containing protein α
Tetratricopeptide Repeat
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Summary:Although androgen therapy resistance and poor clinical outcomes are seen in most canine prostate cancer cases, there are only a few tools for analysing canine prostate cancer by using a cell biological approach. Therefore, to evaluate androgen‐independent neoplastic cell growth, a new canine prostate cancer cell line (CHP‐1) was established in this study. CHP‐1 over‐expressed the co‐chaperone small glutamine‐rich tetratricopeptide repeat‐containing protein α (SGTA), which is over‐expressed in human androgen‐independent prostate cancer. The CHP‐1 xenograft also showed SGTA over‐expression. Although CHP‐1 shows poor androgen receptor (AR) signalling upon dihydrotestosterone stimulation, forced expression of AR enabled evaluation of AR signalling. Taken together, these results suggest that CHP‐1 will be a useful model for investigating the pathogenesis of androgen‐dependent and androgen‐independent canine prostate cancer.
ISSN:1476-5810
1476-5829
DOI:10.1111/vco.12199