SHARPIN overexpression induces tumorigenesis in human prostate cancer LNCaP, DU145 and PC-3 cells via NF-κB/ERK/Akt signaling pathway
SHARPIN overexpression induces tumorigenesis in human prostate cancer LNCaP, DU145 and PC-3 cells via NF-κB/ERK/Akt signaling pathway
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SHARPIN 过表达通过 NF-kappa B/ERK/Akt 信号通路诱导人前列腺癌 LNCaP、DU145 和 PC-3 细胞肿瘤发生
DOI：
10.1007/s12032-014-0444-3
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发表时间：
2015-02-01
期刊：
影响因子：
3.4
通讯作者：
Guo, Zhenghui
中科院分区：
文献类型：
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作者：
Li, Jin;Lai, Yiming;Guo, Zhenghui
我们在前期的研究中通过免疫组化方法发现SHARPIN在前列腺癌组织中的表达高于前列腺增生组织。在这项工作中，我们进行了功能获得试验，发现SHARPIN在LNCaP，DU 145和PC-3细胞中的过表达促进细胞增殖，侵袭力和减少凋亡。此外，SHARPIN过表达显示Bcl-2和Survivin表达升高，Bax、切割的caspase-3水平降低。同时，SHARPIN的熵表达增加了这些细胞中磷酸化的p65、IkB α、ERK和Akt的水平。总的来说，我们的研究揭示了SHARPIN过表达通过NF-κ B/ERK/Akt通路和前列腺增生相关蛋白的转化诱导前列腺癌细胞肿瘤发生的能力。
SHARPIN emerges higher expression in prostate cancerous tissues than in benign prostate hyperplasia by means of immunohistochemistry in our previous study. In this work, we performed the gain of function assay and find that overexpression of SHARPIN in LNCaP, DU145 and PC-3 cells promoted cell proliferation, invasiveness and reduced apoptosis. Furthermore, SHARPIN overexpression displayed elevated Bcl-2 and Survivin expression and reduced levels of Bax, cleaved caspase-3. Meanwhile, entropic expression of SHARPIN increased the levels of phosphorylated p65, IkB alpha, ERK and Akt, were selectively increased in these cells. Collectively, our study unraveled the ability of SHARPIN overexpression to induce tumorigenesis of prostate cancer cells through the NF-kB/ERK/Akt pathway and transformation of apoptosis-associated proteins.