Parnian Vakili, “The Role of Midkine in Pancreatic Cancer Liver Metastasis”
Mentor: Nikki Lytle, MCW (partnership with UWM)
Poster #188
Pancreatic cancer is the third leading cause of cancer deaths in the United States, with metastasis, the spread of cancer cells beyond the original tumor, being the primary cause of mortality. Patients with advanced metastatic disease have a 5-year survival rate below 5%. Studies show that the metastatic tumor microenvironment, which includes surrounding non-cancerous cells, blood vessels, immune cells, and signaling molecules, plays a key role in the progression of metastasis. Midkine (MDK) is a protein involved in various cellular processes and has been studied for its potential involvement in cancer progression. Our lab demonstrated that in a mouse model with accelerated pancreatic metastasis in the liver, MDK expression is increased in liver cells. It remains unknown if MDK contributes to pancreatic cancer metastasis. To address this gap, we aimed to determine whether liver-derived MDK influences tumor cell behavior. Since MDK can bind to several receptors, we assessed which receptors are expressed by human and mouse pancreatic cancer cell lines, as well as whether the cancer cells themselves express MDK. We show that pancreatic cancer cells express and secrete MDK and also express its associated receptors SDC1 and PRKCZ. Further, analysis of publicly available datasets from pancreatic cancer patients reveals that high MDK expression is associated with more aggressive pancreatic cancer, and MDK levels are elevated in liver metastases compared to primary cancer sites. These findings suggest a potential pathway for therapeutic intervention, as we aim to test whether targeting MDK may effectively prevent metastatic progression and improve patient outcomes.