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2
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Cholangiocarcinoma: Current opinion on clinical practice diagnostic and therapeutic algorithms: A review of the literature and a long-standing experience of a referral center.胆管癌:关于临床实践诊断和治疗算法的当前观点:文献综述及转诊中心的长期经验
Dig Liver Dis. 2016 Mar;48(3):231-41. doi: 10.1016/j.dld.2015.11.017. Epub 2015 Nov 28.
2
Prognostic significance of macrophage invasion in hilar cholangiocarcinoma.巨噬细胞浸润在肝门部胆管癌中的预后意义
BMC Cancer. 2015 Oct 24;15:790. doi: 10.1186/s12885-015-1795-7.
3
NHERF1 regulates actin cytoskeleton organization through modulation of α-actinin-4 stability.NHERF1通过调节α-辅肌动蛋白-4的稳定性来调控肌动蛋白细胞骨架的组织。
FASEB J. 2016 Feb;30(2):578-89. doi: 10.1096/fj.15-275586. Epub 2015 Oct 2.
4
Prognostic significance of grading based on the counting of poorly differentiated clusters in colorectal mucinous adenocarcinoma.基于结直肠黏液腺癌中低分化簇计数的分级的预后意义。
Hum Pathol. 2015 Nov;46(11):1722-9. doi: 10.1016/j.humpath.2015.07.013. Epub 2015 Jul 29.
5
Advances in endoscopic retrograde cholangiopancreatography for the treatment of cholangiocarcinoma.内镜逆行胰胆管造影术治疗胆管癌的进展
World J Gastrointest Endosc. 2015 Jun 25;7(7):675-87. doi: 10.4253/wjge.v7.i7.675.
6
The prognostic value of the Na⁺/ H⁺ exchanger regulatory factor 1 (NHERF1) protein in cancer.钠氢交换调节因子1(NHERF1)蛋白在癌症中的预后价值。
Cancer Biomark. 2014;14(2-3):177-84. doi: 10.3233/CBM-130329.
7
Breast cancer-derived K172N, D301V mutations abolish Na+/H+ exchanger regulatory factor 1 inhibition of platelet-derived growth factor receptor signaling.乳腺癌衍生的 K172N、D301V 突变可消除 Na+/H+ 交换体调节因子 1 对血小板衍生生长因子受体信号的抑制作用。
FEBS Lett. 2013 Oct 11;587(20):3289-95. doi: 10.1016/j.febslet.2013.08.026. Epub 2013 Sep 5.
8
Stabilization of the angiotensin-(1-7) receptor Mas through interaction with PSD95.通过与 PSD95 的相互作用稳定血管紧张素-(1-7) 受体 Mas。
Biochem J. 2013 Aug 1;453(3):345-56. doi: 10.1042/BJ20121885.
9
Tumor suppressor function of ezrin-radixin-moesin-binding phosphoprotein-50 through β-catenin/E-cadherin pathway in human hepatocellular cancer.ezrin-radixin-moesin 结合磷蛋白 50 通过 β-连环蛋白/E-钙黏蛋白通路在人肝癌中的抑瘤作用。
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EBP50 inhibits EGF-induced breast cancer cell proliferation by blocking EGFR phosphorylation.EBP50 通过阻断 EGFR 磷酸化抑制 EGF 诱导的乳腺癌细胞增殖。
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EBP50表达水平降低与肝外胆管癌不良临床病理特征相关,并促进QBC939细胞的增殖和迁移。

Reduced EBP50 expression levels are correlated with unfavorable clinicopathological features of extrahepatic bile duct carcinoma and promote the proliferation and migration of QBC939 cells.

作者信息

Feng Duiping, Xiong Ying, Peng Zhiqiang, Ma Qiang, Tao Tao, Liu Hua, Liang Jianfang, Wei Zhigang, Zheng Junfang, Wang Lei, Zhang Hui

机构信息

Department of Radiology, The First Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China.

Beijing Key Laboratory for Tumor Invasion and Metastasis, Cancer Institute of Capital Medical University, Beijing 100069, P.R. China.

出版信息

Oncol Lett. 2017 Apr;13(4):2758-2764. doi: 10.3892/ol.2017.5789. Epub 2017 Feb 28.

DOI:10.3892/ol.2017.5789
PMID:28454463
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5403243/
Abstract

The present study aimed to clarify the association between ezrin-radixin-moesin-binding phosphoprotein-50 (EBP50) expression level and the tumor phenotype and clinicopathological features of extrahepatic bile duct carcinoma. Tissue samples from patients with extrahepatic bile duct carcinoma (54 cases) and patients with normal bile duct epithelia from gallbladder of cholecystitis (20 cases) were collected, and immunohistochemical staining was used to detect the expression levels of EBP50 in these tissues. In addition, small interfering (si)RNA-EBP50 was used to knock down the expression of EBP50 in the QBC939 human cholangiocarcinoma (CC) cell line. The effect of EBP50 expression on QBC939 cell proliferation and migration was analyzed using the Cell Counting kit-8 and wound healing assays, respectively. EBP50 expression was significantly downregulated in CC tissue samples (P<0.01), with low EBP50 expression levels positively correlated with a high pathological stage and a poor differentiation degree (P<0.01 and P<0.001, respectively). EBP50 expression in QBC939 cells was knocked down by ≤80% using siRNA-EBP50, and EBP50 knockdown significantly promoted QBC939 cell proliferation, as compared with the vector control cells (P=0.04). EBP50 knockdown also significantly enhanced the wound healing ability of QBC939 cells (P=0.02). These results demonstrated that EBP50 expression levels are significantly correlated with a malignant phenotype in patients with CC, and decreased expression levels of EBP50 may promote CC cell proliferation and migration. These findings provide insight into novel potential diagnostic and therapeutic approaches for patients with CC.

摘要

本研究旨在阐明埃兹蛋白-根蛋白-膜突蛋白结合磷蛋白50(EBP50)表达水平与肝外胆管癌肿瘤表型及临床病理特征之间的关联。收集了肝外胆管癌患者(54例)和胆囊炎患者胆囊正常胆管上皮患者(20例)的组织样本,采用免疫组织化学染色检测这些组织中EBP50的表达水平。此外,使用小干扰(si)RNA-EBP50敲低QBC939人胆管癌细胞系中EBP50的表达。分别使用细胞计数试剂盒-8和伤口愈合试验分析EBP50表达对QBC939细胞增殖和迁移的影响。EBP50在胆管癌组织样本中的表达显著下调(P<0.01),EBP50低表达水平与高病理分期和低分化程度呈正相关(分别为P<0.01和P<0.001)。使用siRNA-EBP50可将QBC939细胞中EBP50的表达敲低≤80%,与载体对照细胞相比,EBP50敲低显著促进了QBC939细胞增殖(P=0.04)。EBP50敲低还显著增强了QBC939细胞的伤口愈合能力(P=0.02)。这些结果表明,EBP50表达水平与胆管癌患者的恶性表型显著相关,EBP50表达水平降低可能促进胆管癌细胞增殖和迁移。这些发现为胆管癌患者的新型潜在诊断和治疗方法提供了思路。