EDAG-1 promotes the proliferation of human T-acute lymphoblastic leukemia cells by activating MAPK/Erk and Akt signaling pathways
EDAG-1 promotes the proliferation of human T-acute lymphoblastic leukemia cells by activating MAPK/Erk and Akt signaling pathways
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EDAG-1通过激活MAPK/Erk和Akt信号通路促进人急性T淋巴细胞白血病细胞增殖
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
bibo li
中科院分区：
文献类型：
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作者：
bibo li
胚胎发育相关基因1（EDAG-1）是从4个月胎儿肝脏与成人肝脏差异表达基因EST库中发现的一个新基因。前期研究发现EDAG-1在造血组织、胎肝和成人肝组织中差异表达。EDAG-1在T细胞急性淋巴细胞白血病（T-ALL）细胞和T-ALL患者外周血中也有高表达，但其在T-ALL中的功能意义尚不清楚。hu-.man本研究旨在探讨EDAG-1如何参与T-ALL。结果提示EDAG-1在T-ALL细胞和患者外周血中呈高表达。我们发现，敲低EDAG-1可抑制T-ALL细胞的增殖，而过表达EDAG-1则可逆转这一变化。此外，我们发现EDAG-1的过表达可以激活MAPK/Erk和AKT信号通路。我们的研究结果表明EDAG-1在T-ALL的进展中起致癌作用，沉默EDAG-1可能是T-ALL的潜在治疗方法。
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 hu-.man 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.