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• W3149568507 abstract "NF-jB and Akt are two main cell survival pathways that attenuate the anticancer efficacy of thera- peutics. Our previous studies demonstrated that the Smac mimetic compound 3 (SMC3) specifically suppresses c-IAP1 and induces TNF-a autocrine to kill cancer cells. However, SMC3 also induces a cell survival signal through NF-jB activation. In this report, we further found that SMC3 potently activates Akt, which inhibits SMC3- induced cancer cell death. Strikingly, concurrent blocking NF-jB and Akt resulted in a significantly potentiated cytotoxicity. Because heat shock protein 90 (Hsp90) plays an important role in maintaining the integrity of both the NF-jB and Akt pathways in cancer cells, we examined if suppression of Hsp90 is able to potentiate SMC3-induced cancer cell death. The results show that targeting Hsp90 does not interfere with SMC3-induced c-IAP1 degradation and TNF-a autocrine, the key processes for SMC3-induced cancer cell apoptosis. However, Hsp90 inhibitors effec- tively blocked SMC3-induced NF-jB activation through degradation of RIP1 and IKKb, two key components of the NF-jB activation pathway, and reduced both the constitutive and SMC3-induced Akt activity through degradation of the Akt protein. Consistently, with the co-treatment of SMC3 and Hsp90 inhibitors, apoptosis was markedly sensitized and a synergistic cytotoxicity was observed. The results suggest that concurrent targeting c-IAP1 and Hsp90 by combination of SMC3 and Hsp90 inhibitors is an effective approach for improving the anticancer value of SMC3." @default.
• W3149568507 created "2021-04-13" @default.
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• W3149568507 date "2011-01-01" @default.
• W3149568507 modified "2023-09-26" @default.
• W3149568507 title "Blocking NF-jB and Akt by Hsp90 inhibition sensitizes Smac mimetic compound 3-induced extrinsic apoptosis pathway and results in synergistic cancer cell death" @default.
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