中文摘要：

锌手指蛋白质 X 连接(ZFX ) 是胚胎的干细胞(转换字符) 和造血的干细胞(HSC ) 的一个关键管理者，它被要求因为两个都槽口细胞内部的领域(NotchIC ) 在鼠标模型导致了尖锐 T 房间白血病和 MLL-AF9-induced myeloid 白血病。然而， ZFX 的角色和它在人的白血病的房间的内在的机制还仍然保持不清楚，尽管积累的数据证明了 ZFX 异常地在各种各样的人的肿瘤被表示并且起一个重要作用。此处，我们发现 ZFX 异常地与控制房间相比从白血病病人在各种各样的人的白血病的房间线和主要房间被表示。ZFX 的沉默包括 K562， Jurkat， Namalwa，和 THP-1 房间在各种各样的房间通过 deregulated 房间周期或 apoptosis 的正式就职导致了生长抑制。基因表示分析揭示了那 UDP 女郎: GlcNAc 1,4-galactosyltransferase，(B4GALT1 ) 多肽 1 在 ZFX silencing 之上是显著地下面调整的，它在对 imatinib mesylate (IM ) 的治疗的 K562 房间的反应被含有。另外， lectin 污点试金证明在 K562 房间的 glycoproteins 的 galactosylation 在 ZFX silencing 之上被压制。有趣地， B4GALT1 的 overexpression 恢复了生长并且授与药抵抗到沉默 ZFX 的细胞。一起拿，我们证明了 ZFX 异常地在多重人的白血病的房间被表示，它经由 B4GALT1 部分调制生长和白血病的房间的药反应，它建议 ZFX 是白血病的房间的一个新管理者并且在这些致命的疾病在这个 stemness 管理者上保证集中的调查。

英文摘要：

Zinc finger protein X-linked （ZFX） is a key regulator of both embryonic stem cells （ESCs） and hematopoietic stem cells （HSCs）, which is required for both Notch intracellular domain （NotchlC）- induced acute T-cell leukemia and MLL-AF9-induced myeloid leukemia in mouse models. However, the role of ZFX and its underlying mechanism in human leukemic cells remain unclear yet, though accumulating data have demonstrated that ZFX is aberrantly expressed in various human tumors and plays an important role. Herein, we found that ZFX was aberrantly expressed in various human leukemic cell lines and primary cells from leukemia patients compared with control cells. The silence of ZFX led to the growth suppression through either the deregulated cell cycle or the induction of apoptosis in various cells including K562, Jurkat, Namalwa, and THP-1 cells. The gene expression analysis revealed that UDP-GaI：βGIcNAc β 1,4-galactosyltransferase, polypeptide 1 （B4GALT1） was significantly down-regulated upon ZFX silencing, which is impli- cated in the response of K562 cells to the treatment of imatinib mesylate （IM）. In addition, lectin blot assay showed that the galactosylation of glycoproteins in K562 cells was suppressed upon ZFX silencing. Interestingly, overexpression of B4GALT1 restored the growth and conferred drug resistance to ZFX-silenced cells. Taken together, we have demonstrated that ZFX is aberrantly expressed in multiple human leukemic cells and it modulates the growth and drug response of leukemic cells partially via B4GALT1, which suggests that ZFX is a new regulator of leukemic cells and warrants intensive investigations on this ＇stemness＇ regulator in these deadly diseases.