Natalie Pedroza
Research Mentor: Siva Kumar Natarajan
Mentor Department: Department of Pathology, Medicine
Author(s): Not Available
Session: Session 5 (2:00 PM – 2:50 PM)
Presentation Type: Poster 49
Abstract
Prostate cancer is the second leading cause of cancer-related death among men in the United States, with 1 in 8 men diagnosed in their lifetime. Androgens, such as testosterone and dihydrotestosterone (DHT), promise prostate cancer by binding and activating the androgen receptor (AR) in tumor cells. Upon activation, AR translocates to the nucleus, where it functions as a transcription factor to enhance cell survival, proliferation, and tumor growth. In oxygen-deprived environments, prostate cancer cells convert glucose to pyruvate via glycolysis. Pyruvate can then be converted to lactate through lactic acid fermentation, catalyzed by lactate dehydrogenase A (LDHA), while lactate can be converted back to pyruvate by lactate dehydrogenase B (LDHB). Analysis of the Cancer Dependency Map (DepMap) database indicates that AR and LDHA are positively correlated and essential for survival in multiple prostate cancer cell lines. Similar results were observed in comparisons of AR and LDHB. Cell viability assays demonstrate that prostate cancer cell lines are more likely to survive in the presence of lactate, even when deprived of other metabolites, with comparable results seen when cells are maintained with only glucose. Our hypothesis is that lactate acts as an important metabolite in the survival of prostate cancer cells. Further research will investigate the interactions between AR signaling and lactate metabolism.
