Mechanism and therapeutic significance of ARV-110 combined with a PDGFR inhibitor for the induction of apoptosis in castration-resistant prostate cancer cells through the ROS/JNK pathway - PubMed
3 hours ago
- #castration-resistant prostate cancer
- #combination therapy
- #ARV-110
- The study investigates a combination therapy using ARV-110 (an AR degrader) and PDGFR inhibitors (e.g., ponatinib, JNJ10198409) to treat castration-resistant prostate cancer (CRPC) by targeting both AR-dependent and independent pathways.
- Combination treatment significantly inhibits CRPC cell viability and induces apoptosis through synergistic effects, activating the ROS/JNK pathway and downregulating catalase to increase reactive oxygen species accumulation.
- Mechanistic insights reveal ARV-110 promotes PDGFA transcription, and combining it with PDGFR inhibitors further activates JNK signaling and inhibits PDGFR activity, offering a new precision therapeutic strategy for CRPC.