|Education||BS. University of Maryland College Park|
Metastatic prostate cancer (PCa) incites tremendous morbidity; yet the mechanisms driving metastatic progression in the prostate are not well understood. As the tumor microenvironment influences PCa progression, we hypothesized that molecules secreted by cancer associated fibroblasts (CAFs) in the primary tumor could modulate tumor progression and predict metastatic potential. We previously reported that Asporin (ASPN), a member of the small leucine-rich proteoglycan (SLRP) family of extracellular proteins, was one of the most highly enriched mesenchymal genes during both physiologic development and pathologic growth in the prostate. Most intriguingly, we have demonstrated that while ASPN is expressed at low levels in benign associated stroma, it is highly expressed by CAFs in the tumor microenvironment. In addition, ASPN expression is significantly associated with adjacent cancer aggressiveness as measured by Gleason grade, and with worse oncologic outcomes including metastatic progression. Similar to that seen in PCa, ASPN is upregulated in multiple solid malignancies including breast, colorectal, gastric, and pancreatic cancer, suggesting that it plays a conserved and critical role in cancer biology. Therefore, elucidating ASPN’s function will provide opportunities for improving prognosis and therapy in many types of cancer.