Evaluating the Role and Therapeutic Value of MAP1B in Prostate Cancer

Prostate cancer (PCa) is commonly treated by blocking male hormone signaling through suppression of testosterone production or blocking its binding to its main cellular receptor. While these treatments initially suppress disease progression, the cancer often develops resistance and recurs. In about 20% of cases, the disease returns as an aggressive and lethal form known as neuroendocrine prostate cancer (NEPC), which is associated with a median survival of under one year. There is an urgent need to define the mechanisms driving treatment resistance and NEPC progression. Our lab has identified a protein, MAP1B, that is upregulated in response to treatment stress and is highly expressed in NEPC. Suppressing MAP1B expression reduced cancer cell growth, decreased cell movement, and led to a loss of neuroendocrine-like features, suggesting that MAP1B may play a critical role in treatment resistance and NEPC progression. We plan to investigate how MAP1B is upregulated following treatment stress and how it promotes NEPC progression. We will also assess whether suppressing MAP1B slows NEPC tumor growth in an animal model. With these studies, we aim to uncover a biomarker for treatment-induced NEPC and a therapeutic target in advanced PCa.