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EDAG-1 promotes the proliferation of human T-acute lymphoblastic leukemia cells by activating MAPK/Erk and Akt signaling pathways
被引:0
|作者:
He, Daiying
[1
]
Luo, Zhibin
[1
]
Li, Bibo
[1
]
He, Mei
[2
]
Xia, Kanji
[1
]
Li, Jing
[1
]
Wang, Chen
[1
]
Wu, Yuni
[1
]
Xu, Yizhi
[1
]
机构:
[1] Chongqing Gen Hosp, Dept Oncol & Hematol, 104 Pipashan Rd, Chongqing 400014, Peoples R China
[2] Chongqing Canc Inst Hosp Ctr, Off Canc Prevent & Control, 181 Hanyu Rd, Chongqing 400030, Peoples R China
来源:
基金:
中国国家自然科学基金;
关键词:
EDAG-1;
T-acute lymphoblastic leukemia cells;
MAPK/Erk;
Akt;
APOPTOSIS;
DIFFERENTIATION;
EXPRESSION;
KNOCKDOWN;
LINE;
NPM1;
D O I:
暂无
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Embryonic develop associated gene 1 (EDAG-1) is a novel gene identified from the EST bank of differently expressed genes between the 4 months fetal liver and adult liver. Previous studies found that EDAG-1 differentially expressed in hematopoietic tissues, fetal liver and adult liver tissues. High EDAG-1 expression is also found in human T-cell acute lymphoblastic leukemia (T-ALL) cells and peripheral blood of patients with T-ALL, but its functional significance in T-ALL was unclear. This present study aimed to investigate how EDAG-1 is involved in T-ALL. Our results suggested that EDAG-1 was highly expressed in T-ALL cells and peripheral blood of patients with T-ALL. We found that knockdown of EDAG-1 could inhibit the proliferation of T-ALL cells, whereas overexpression of EDAG-1 reversed this change. Furthermore, we found that overexpression of EDAG-1 could activate the MAPK/Erk and AKT signal pathways. Our findings demonstrated that EDAG-1 should play an oncogenic role in T-ALL progression and silencing EDAG-1 might be a potential therapeutic approach for T-ALL.
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页码:4173 / 4181
页数:9
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