Prostate cells have a unique metabolic profile to produce and secrete large quantities of citrate. During the development of prostate cancer, a significant metabolic reprogramming takes place, but the underlying mechanisms are not yet known. By understanding how this reprogramming occurs, or what vulnerabilities it causes, we could restore the metabolic balance in tumor cells to treat prostate cancer.
My recent research has highlighted the importance of the androgen receptor in establishing a genomic program to control the metabolism of prostate cancer cells. My first research axis will be to dissect this program to identify the underlying metabolic vulnerabilities established by this receptor. In parallel, my work showed that estrogens and their receptors are also intimately linked to the development and progression of prostate cancer. I am therefore interested in understanding in more detail how these receptors will change the activity of tumor cells, including how they will alter the activity of the androgen receptor and thus promote or block the progression of prostate cancer. I am particularly interested in their actions on cellular metabolism to identify potential vulnerabilities that would be put into place in tumor cells.
In summary, I am interested in two major research questions. First, how do the androgen and estrogen receptors reprogram tumor cell metabolism? Second, can we identify the metabolic vulnerabilities linked to the activity of these hormone receptors? My long-term goal is to use this knowledge to develop new therapeutic approaches targeting the unique metabolism of prostate cancer cells.