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Overexpression of multidrug resistance proteins (Mdrs) and enhanced antiapoptotic capability are two of the main mechanisms by which  Bcr/Abl  +  chronic myeloid leukemia cells acquire drug resistance; however, it has been shown that Mdr-1 expression provides minimal protection against cell apoptosis induced by chemotherapeutic drugs. The mechanism by which cells acquire an enhanced antiapoptosis capacity in the drug-resistant process needs to be further understood. Here, we identified human brain expressed X-linked 1 ( hBex 1) as a downstream target of the p75 neurotrophin receptor pathway in imatinib-resistant K562 cells by comparing the gene expression profiles with the parent K562 cells. Silencing  hBex 1 inhibited imatinib-induced cell apoptosis and overexpression of hBex1-sensitized cells to imatinib-induced apoptosis. Further investigation revealed that hBex1 associates with protocadherin 10 (PCDH10). Silencing of  pcdh 10 attenuated apoptosis induced by imatinib in  hBex 1 transfected cells, suggesting that, in addition to Mdr and Bcl-2 family members, reduced expression of hBex1 can also inhibit imatinib-induced apoptosis. These data provide evidence that expression of hBex1 in leukemic cells is a novel mechanism by which chemoresistance is achieved and suggests that hBex1 is a potential molecular target for the development of novel leukemia treatments.

Inhibition of apoptosis by downregulation of hBex1, a novel mechanism, contributes to the chemoresistance of Bcr/Abl + leukemic cells