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• W2172152078 abstract "Caspase-3 downregulation (CASP3/DR) in tumors frequently confers resistance to cancer therapy and is significantly correlated with a poor prognosis in cancer patients. Because CASP3/DR cancer cells rely heavily on the activity of caspase-7 (CASP7) to initiate apoptosis, inhibition of activated CASP7 (p19/p12-CASP7) by X-linked inhibitor of apoptosis protein (XIAP) is a potential mechanism by which apoptosis is prevented in those cancer cells. Here, we identify the pocket surrounding the Cys246 residue of p19/p12-CASP7 as a target for the development of a protein-protein interaction (PPI) inhibitor of the XIAP:p19/p12-CASP7 complex. Interrupting this PPI directly triggered CASP7-dependent apoptotic signaling that bypassed the activation of the apical caspases and selectively killed CASP3/DR malignancies in vitro and in vivo without adverse side effects in nontumor cells. Importantly, CASP3/DR combined with p19/p12-CASP7 accumulation correlated with the aggressive evolution of clinical malignancies and a poor prognosis in cancer patients. Moreover, targeting of this PPI effectively killed cancer cells with multidrug resistance due to microRNA let-7a-1-mediated CASP3/DR and resensitized cancer cells to chemotherapy-induced apoptosis. These findings not only provide an opportunity to treat CASP3/DR malignancies by targeting the XIAP:p19/p12-CASP7 complex, but also elucidate the molecular mechanism underlying CASP3/DR in cancers." @default.
• W2172152078 created "2016-06-24" @default.
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• W2172152078 date "2013-08-27" @default.
• W2172152078 modified "2023-10-10" @default.
• W2172152078 title "Targeting the XIAP/caspase-7 complex selectively kills caspase-3–deficient malignancies" @default.
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• W2172152078 doi "https://doi.org/10.1172/jci67951" @default.
• W2172152078 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3754255" @default.
• W2172152078 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23979166" @default.
• W2172152078 hasPublicationYear "2013" @default.
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