MOLECULAR DISSECTION OF WNT SIGNALING IN THE PCSD NEW SERIES OF PATIENT-DERIVED XENOGRAFT MODELS OF BONE METASTATIC PROSTATE CANCER
Theresa Mendoza1, Danielle Burner1, Michelle Muldong1, Amy Strasner1, Christina Wu1, Seung Chol Park1, Elana Godebu1, Omer Raheem1, Catriona Jamieson1, Colm Morissey2, Isaac Kim3, Anna Kulidjian1, Christina Jamieson1.
1University of California, San Diego, La Jolla,, CA, 2University of Washington, Seattle, WA, 3Rutgers Cancer Institute of New Jersey, New Brunswick, NJ.
One of the leading health problems affecting men in the U.S. and many other parts of the world is prostate cancer. Cancer patients are surviving longer due to androgen deprivation therapies. However, over 80% of advanced patients develop bone metastatic prostate cancer for which there is no cure. Therefore, the goal of this project is to determine which signaling components would serve as potential targets for bone metastatic prostate cancer therapy using our lab’s new prostate cancer xenograft models. Researchers have shown that the WNT signaling pathway regulates various processes that are important for cancer progression including tumor initiation, tumor growth, cell death, differentiation, and metastasis. Thus, it is hypothesized that the WNT signaling componentsWNT5A, BMP-6, and ROR receptors help prostate cancer thrive and become aggressive in the bone microenvironment in the absence of androgen. To determine whether these WNT signaling components were expressed at the RNA level in our lab’s prostate cancer xenograft models, reverse transcriptase polymerase chain reactions (RT PCR) have been performed. The results of the experiments showed that BMP-6, ROR1, and WNT5A components are expressed in our prostate cancer xenograft models. Further testing using real time PCR (qPCR) and immunohistostaining assays will be done in the future and, if the results of these experiments indicate that the WNT signaling pathway could potentially serve as an effective target for therapy, we would then utilize knock-out and overexpression methods on our prostate cancer xenograft models.