Yes, targeting the UPR is a promising strategy for cancer therapy. Several approaches are being explored:
Inhibiting UPR pathways: Small molecule inhibitors targeting PERK, IRE1, or ATF6 can disrupt the adaptive UPR, leading to increased apoptosis in cancer cells. Modulating chaperone activity: Drugs that inhibit molecular chaperones like Hsp90 can exacerbate ER stress, pushing cancer cells towards cell death. Exploiting UPR-induced vulnerabilities: Combining UPR inhibitors with other therapies (e.g., chemotherapy) can enhance treatment efficacy by exploiting the stress response mechanisms in cancer cells.
