ZFX Facilitates Cell Proliferation and Imatinib Resistance in Chronic Myeloid Leukemia Cells

被引:10
作者
Wu, Jingjing [1 ]
Wei, Bin [2 ]
Wang, Qian [1 ]
Ding, Yihan [1 ]
Deng, Zhikui [1 ]
Lu, Xueying [1 ]
Li, Yufeng [1 ]
机构
[1] Nanjing Med Univ, Huaian Peoples Hosp 1, Dept Hematol, Huaian 223300, Peoples R China
[2] Nanjing Med Univ, Huaian Peoples Hosp 1, Dept Oncol, Huaian 223300, Peoples R China
关键词
ZFX; CML; Proliferation; Imatinib; PI3K/Akt; CHRONIC MYELOGENOUS LEUKEMIA; SELF-RENEWAL; BCR-ABL; CYCLE PROGRESSION; TYROSINE KINASE; K562; CELLS; IN-VITRO; KNOCKDOWN; CARCINOMA; GROWTH;
D O I
10.1007/s12013-016-0725-x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Zinc finger protein, X-linked (ZFX) mediates the development and progression of human cancers. However, its potential role in chronic myeloid leukemia (CML) is still unknown. The ZFX expression was significantly increased in CML patients and cell lines. Based on loss-of-function experiments in CML cells, we found that knockdown of ZFX expression impaired cell proliferation and induced mitotic arrest in G0/G1 stage and apoptosis. In addition, ZFX silencing sensitized CML cells to imati nib treatment. Further, phospho-Akt (p-Akt), CyclinD1, CyclinE1, and Bcl-2 were downregulated, and Caspase-3 was upregulated in ZFX-silenced cells. In summary, our data suggest that ZFX is a novel oncogene promoting cell proliferation and inducing imatinib resistance via PI3K/Akt signaling pathway. ZFX may represent a potential therapeutic target in CML.
引用
收藏
页码:277 / 283
页数:7
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