Paxillin may become a therapeutic target in treatment-resistant prostate cancer, based on new research demonstrating that this protein can regulate signals that lead to the creation of cancer cells even in the absence of tumor-nurturing hormones.
“The holy grail in prostate cancer is to figure out why cells stop responding to hormone therapy,” explained Stephen R. Hammes, MD, PhD, to describe the importance of his team’s discovery, in a statement issued by the University of Rochester Medical Center in Rochester, New York. Hammes is chief of the Division of Endocrinology and Metabolism at the medical center.
In typical prostate tumors fueled by male hormones, paxillin collaborates with these androgens to stimulate genes that help breed more cancer cells. When subjected to hormone therapy, such tumors shrink, at least for a time. However, “Somehow, tumors find a way to grow even when their main power source [androgens] is choked off,” noted Hammes.
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Hammes and colleagues appear to have found a reason for this, as they reported in The Journal of Clinical Investigation (2012;122[7]:2469-2481): The group showed that paxillin regulates both androgen-induced and epidermal growth factor (EGF)-induced nuclear signaling in a cell, and that androgens and EGF promote a process that allows paxillin to enter the cell’s nucleus. From that command center, paxillin is able to control gene expression and help cancer cells to develop, bypassing the need for hormones.
Eliminating paxillin from prostate cancer cells significantly arrested the growth of those cells, making the protein a possible biomarker for prostate cancer proliferation as well as a potential target for treatment.
