| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2048559 | FEBS Letters | 2009 | 8 Pages |
SNX-2112, a novel inhibitor of Hsp90 currently used as an anti-tumor drug, induces apoptosis in multiple tumor cell lines. It destabilizes specific client proteins, but the molecular mechanism of the apoptosis effect of SNX-2112 is poorly understood. Here, we analyzed the apoptotic effect of SNX-2112 on human chronic myeloid leukemia (CML) K562 cells. Transcriptomic and proteomic approaches further revealed that caspase signals originated from mitochondria dysfunction, mediated by Akt signaling pathway inactivity. Additionally, SNX-2112 prolonged the survival time of NOD/SCID mice inoculated with K562 tumor cells. Our results demonstrated the therapeutic potential of SNX-2112 against human CML.Structured summaryMINT-7033976: BAD (uniprotkb:Q92934) physically interacts (MI:0218) with Bcl2-Xl (uniprotkb:Q07817) by anti bait coimmunoprecipitation (MI:0006)
