Paip1 predicts poor prognosis and promotes tumor progression through AKT/GSK-3β pathway in Lung adenocarcinoma
Paip1 predicts poor prognosis and promotes tumor progression through AKT/GSK-3β pathway in Lung adenocarcinoma
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Paip1 通过 AKT/GSK-3 β 通路预测肺腺癌的不良预后并促进肿瘤进展
DOI：
10.1016/j.humpath.2018.11.017
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发表时间：
2019-04-01
期刊：
影响因子：
3.3
通讯作者：
Lin, Zhenhua
中科院分区：
文献类型：
--
作者：
Wang, Yixuan;Piao, Junjie;Lin, Zhenhua
在大多数人类癌症中，Paip1的表达和生物学功能仍然知之甚少。本研究旨在探讨其在肺腺癌（LADC）中的临床意义和作用。采用免疫组化方法检测58例严格随访的LADC患者及60例相邻正常肺组织中Paip1的表达。与邻近正常肺组织相比，77.6%（45/58）的LADC组织中Paip1蛋白表达上调。Paip1过表达与组织学分级、临床分期及预后不良有显著相关性。小干扰rna介导转染A549和H1299细胞。pap1的缺失降低了A549和H1299细胞的增殖和迁移。Paip1还改变了上皮到间质转化标记物的表达，包括E-cadherin、Vimentin、Slug和Snail。此外，Paip1调节AKT/GSK-3 β致癌信号通路。综上所述，在LADC中，Paip1的表达频繁上调，其过表达与LADC患者预后不良相关。减弱的Paip1表达通过调节AKT/GSK-3 β信号通路抑制A549和H1299细胞的增殖和上皮向间质过渡相关的迁移。(C) 2018爱思唯尔公司版权所有。
The expression and biological function of Paip1 remain poorly understood in most human cancers. The objective of this research is to investigate its clinical significance and roles in lung adenocarcinoma (LADC). Immunohistochemistry was used to determine Paip1 expression in 58 cases of LADC patients with strict follow-up and 60 cases of adjacent normal lung tissues. Paip1 protein was upregulated in 77.6% (45/58) LADC tissues compared with adjacent normal lung tissues. The overexpression of Paip1 was significantly correlated with histologic grade, clinical stage, and poor prognosis. Small interfering RNA-mediated transfection was performed in A549 and H1299 cells. Paip1 depletion attenuated the proliferation and migration of A549 and H1299 cells. Paip1 also changed the expression of epithelial-to-mesenchymal transition markers including E-cadherin, Vimentin, Slug, and Snail. Furthermore, Paip1 regulated AKT/GSK-3 beta oncogenic signaling pathways. In conclusions, Paip1 expression is frequently upregulated in LADC, and its overexpression correlates with poor prognosis in LADC patients. Attenuated Paip1 expression suppresses proliferation and epithelial-to-mesenchymal transition-related migration of A549 and H1299 cells by regulating the AKT/GSK-3 beta signaling pathway. (C) 2018 Elsevier Inc. All rights reserved.