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Anaphase promoting complex cofactor Cdh1 plays a critical role in tumorsuppression and genomic stability in cancer. However, its role in chronic myeloidleukemia (CML) remains unclear. We treated both wild-type and imatinib-resistantK562 cells with imatinib or nilotinib and bortezomib, respectively. The siRNAsof Cdh1 and Skp2 were designed and transiently transfected with HiPerFect transfectionreagent into CML cells. Expression of Cdh1-Skp2-p27 pathway proteins were detectedby Western blotting. Cell cycle, cell apoptosis and cellular morphology were detectedby flow cytometry and Wright staining. Our study revealed that Cdh1 was expressedat lower levels in imatinib-resistant CML blast crisis (BC) patients than imatinib-sensitiveones. Moreover, imatinib and bortezomib induced cell cycle quiescence or arrest,upregulation and nuclear relocation of Cdh1 in CML cells. Furthermore, nilotiniband bortezomib resulted in upregulation of Cdh1 in imatinib-resistant CML cells.Conversely, Cdh1 silencing resulted in stabilization of Skp2 and Cdc20, subsequentlypromoting G1-S transition and formation of multinucleated cells. Our study showsthat TKIs and bortezomib can regulate the cell cycle and cell apoptosis via regulationof the expression and redistribution of Cdh1 in CML-BC, which sheds light on theorchestration of crosstalk between TKIs and bortezomib in imatinib-resistant CML-BC.Additionally, Cdh1 tends to play an important role in maintenance of genomic stability,the detailed mechanisms deserve further study.

international journal of oncology

Imatinib and bortezomib induce the expression and distribution of anaphase-promoting complex adaptor protein Cdh1 in blast crisis of chronic myeloid leukemia