Abstract 1890: Calcitonin receptor is required for T-antigen-induced prostate carcinogenesis

Calcitonin & calcitonin receptor axis (CT-CTR) expression is increased in prostate cancer & its levels positively correlate with Gleason grade of prostate cancer. Moreover, activation of CT-CTR autocrine axis promotes several processes with tumor progression such as, tumor growth, invasion, angiogenesis, chemoresistance & metastasis. However, the role of CT-CTR axis in carcinogenesis process has not been investigated. To examine the role of CT-CTR axis in prostate carcinogenesis we examined the impact of CTR deficiency on T-antigen-induced prostate tumorigeneses in transgenic mice. We achieved this by cross-breading CTR-knockout mice with LPB-Tag mice (the transgenic mice that uses long Probasin promotor for prostate-specific expression of Tag T-antigen). The cross-breeding of these two transgenic mice yielded four different groups of mice with the following genotypes 1. Control (which lacked both transgenes), 2. CTRKO (only CTRKO transgene), 3. LPB-Tag (contained LPB-Tag transgene), & 4. CTRKO-LPB-Tag (expressed Both CTRKO & LPB-Tag transgenes). The growth of these mice were monitored until they reached the age of 90 days. The mice were sacrificed, the prostates were collected, fixed & evaluated by histology & immunohistochemistry. The results suggest that the mice of all groups developed normally with the exception of LPB-Tag group which displayed slower growth & the presence of prostatic tumors at the time of necropsy. Although all LPB-Tag mice displayed all prostate tumors, as expected wild type & CTRKO mice did not display change in the size or mass of prostates. Subsequently, HE 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 1890.