Poster #: 105
The Contribution of Autophagy to Radioresistance in CRPC
Mentor: Kenichi Kudo, Post-Doc
Prostate cancer (PCa) is the second leading cause of cancer-related death in men worldwide. The first-line treatment for PCa involves androgen-deprivation therapy, which blocks androgen receptor (AR) activation. However, a more aggressive form termed castration-resistant prostate cancer (CRPC) may develop radioresistance through AR activation independent of androgen, contributing to tumor progression and propensity for distant metastasis. Based on previous studies, we hypothesize that autophagy promotes radioresistance in CRPC cells, and that inhibiting autophagy through knockdown of autophagy-related (ATG) genes may increase radiosensitivity. We will conduct siRNA-knockdown experiments targeting ATG genes ATG2A, MAP1LC3, and BECN1 in AR-positive PCa cell lines LNCaP and C4-2B to evaluate the role of autophagy in radioresistance. We expect low cell viability and increased levels of apoptotic markers in ATG siRNA-treated groups compared to scramble siRNA-treated groups post-irradiation, indicating increased radiosensitivity. Studying the relationship between autophagy and radioresistance may lead to development of novel therapeutics targeting CRPC.