Enah overexpression is correlated with poor survival and aggressive phenotype in gastric cancer.

Enah overexpression is correlated with poor survival and aggressive phenotype in gastric cancer.
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Enah 过度表达与胃癌的不良生存率和侵袭性表型相关

DOI:
10.1038/s41419-018-1031-x
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发表时间:
2018-09-24
影响因子:
9
通讯作者:
Ren G
Ren G
中科院分区:
生物学1区
文献类型:
--
作者:
Chen D;Xu L;Li X;Chu Y;Jiang M;Xu B;Zhao M;Wang W;Wang H;Kang H;Wang K;Wu K;Liang J;Ren G

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Enable Homolog(Enah)是果蝇Enable(Ena)的哺乳动物同源基因,是Ena/Vasp家族的成员,该家族还包括Vasp(血管扩张剂刺激的磷蛋白)和Ena/Vasp like。越来越多的研究表明,Enah过表达与人类结直肠癌、乳腺癌和肝细胞癌有关。然而,Enah在胃癌中的表达意义尚不清楚。在这里,我们证明了Enah在GC中表达上调,并与AJCC分期、侵袭深度和总体生存不良(OS)相关。Enah基因敲除可抑制GC细胞的增殖和转移,反之亦然。进一步的实验表明,Enah沉默后,p-ERK1/2、p-AKT、p-P65、Vimentin和FN表达下调,E-cadherin表达上调,提示其在胃癌增殖和转移中的作用发生了改变。因此,我们的研究表明,Enah是一种对GC有害的因子,是治疗GC的新靶点。
Enabled homolog (Enah), which is a member of the Ena/VASP family that also includes VASP (vasodilator-stimulated phosphoprotein) and Ena/VASP like, is a mammalian ortholog of Drosophila Enabled (Ena). An increasing number of studies demonstrated Enah overexpression is involved in human colorectal carcinomas, breast cancers and hepatocellular carcinoma. However, the significance of Enah expression in gastric cancer (GC) is poorly elucidated. Here, we demonstrate that Enah is upregulated in GC and associated with AJCC stage, depth of invasion and poor overall survival (OS). Knockdown of Enah inhibited GC cell proliferation and metastasis and vice versa. Further experiments suggested that p-Erk1/2, p-AKT, p-p65, Vimentin and Fibronectin were downregulated and E-cadherin was upregulated after Enah silencing, implicating altered functions in GC proliferation and metastasis. Thus, our study suggests that Enah is a harmful factor for GC and a novel target for GC treatment.
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