The importance of molecular chaperones in cancer is well established, yet several chaperone inhibitors have failed in clinical trials due to toxicity. Recent efforts have focused on targeting chaperone function in cancer by either manipulating the “chaperone code” or inhibiting helper cochaperones, such as DNAJA1. Tong et?al. identify a novel inhibitor that specifically disrupts DNAJA1's interaction with p53, promoting p53 degradation. This finding highlights specific DNAJA1 interactions with the potential for less toxicity compared to traditional chaperone inhibitors.
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