Suppr超能文献

[Kindlin-2通过诱导上皮-间质转化促进胆囊癌转移和侵袭]

[Kindlin-2 promotes gallbladder cancer metastasis and invasion by inducing epithelial-mesenchymal transition].

作者信息

Lu X, Zhou C, Li R F, Ye J W, Zhai W L

机构信息

Department of Hepatobiliary and Pancreatic Surgery, the First Affiliated Hospital of Zhengzhou University, Digestive Organ Transplantation of Henan Province, Zhengzhou 450052, China.

出版信息

Zhonghua Wai Ke Za Zhi. 2018 Aug 1;56(8):617-622. doi: 10.3760/cma.j.issn.0529-5815.2018.08.013.

Abstract

To investigate the effects of Kindlin-2 on malignant phenotypes of human gallbladder cancer cells and discuss the mechanisms. The expression level of Kindlin-2 in 30 cases of gallbladder cancer tissues and adjacent non-tumoral tissues collected from the First Affiliated Hospital of Zhengzhou University between September 2012 and May 2013 was assessed by real-time PCR and immunohistochemistry.Lentivirus-mediated Kindlin-2 overexpression was used in gallbladder cancer cell lines GBC-SD and SGC-996.Transwell assay and adhesion assay were investigated to explore the functional role of Kindlin-2 on gallbladder cancer cells.Western Blot was used to test the protein change of epithelial-mesenchymal transition(EMT) characteristics. The -test was used to analyzed results. The RNA and protein levels of Kindlin-2 in gallbladder cancer tissues were higher than in the non-tumoral tissues (=4.372, =0.001; =7.477, =0.000). The expression level of Kindlin-2 in gallbladder cancer tissues was correlated with Nevin stage(χ(2)=5.932, =0.035). Compared with control groups, the cell-matrix adhesion ability of GBC-SD and SGC-996 with Kindlin-2 overexpression was obviously promoted(1.66±0.03 . 1.07±0.22, =2.710, =0.041; 2.66±0.24 . 1.03±0.02, =6.610, =0.020). The number of GBC-SD and SGC-996 cells with Kindlin-2 overexpression passing through the Transwell chamber matrix increased significantly compared with the control groups(116.1±13.9 . 54.7±8.4, =3.781, =0.019; 136.3±7.5 . 64.3±6.4, =7.302, =0.002). The wound healing rate of GBC-SD with Kindlin-2 overexpression at 12-hour and 24-hour was higher than that of the group ((42.9±2.2)% . (29.7±1.7)%, =4.690, =0.009; (65.0±2.4)% .(40.4±2.0)%, =7.945, =0.001). The wound healing rate of SGC-996 with Kindlin-2 overexpression at 12-hour and 24-hour was also higher than that of the group ((32.9±1.3)% . (24.1±1.5)%, =4.518, =0.011; (51.3±1.1)% . (39.2±1.1)%, =8.001, =0.001). The characteristics of EMT were induced in gallbladder cancer cells with Kindlin-2 overexpression, including the up-regulation of N-cadherin, Vemintin and the down-regulation of E-cadherin. The expression of Kindlin-2 is up-regulated in gallbladder cancer tissues and Kindlin-2 promoted the malignant phenotypes of gallbladder cancer cells partially by epithelial-mesenchymal transition.

摘要

探讨Kindlin-2对人胆囊癌细胞恶性表型的影响并探讨其机制。采用实时荧光定量PCR和免疫组织化学方法检测2012年9月至2013年5月郑州大学第一附属医院收集的30例胆囊癌组织及癌旁非肿瘤组织中Kindlin-2的表达水平。采用慢病毒介导的Kindlin-2过表达技术处理胆囊癌细胞系GBC-SD和SGC-996。通过Transwell实验和黏附实验探讨Kindlin-2对胆囊癌细胞的功能作用。采用蛋白质免疫印迹法检测上皮-间质转化(EMT)相关蛋白的变化。采用t检验分析结果。胆囊癌组织中Kindlin-2的RNA和蛋白水平均高于癌旁非肿瘤组织(t=4.372,P=0.001;t=7.477,P=0.000)。Kindlin-2在胆囊癌组织中的表达水平与Nevin分期相关(χ²=5.932,P=0.035)。与对照组相比,过表达Kindlin-2的GBC-SD和SGC-996细胞与基质的黏附能力明显增强(1.66±0.03比1.07±0.22,t=2.710,P=0.041;2.66±0.24比1.03±0.02,t=6.610,P=0.020)。过表达Kindlin-2的GBC-SD和SGC-996细胞穿过Transwell小室基质的数量较对照组明显增加(116.1±13.9比54.7±8.4,t=3.781,P=0.019;136.3±7.5比64.3±6.4,t=7.302,P=0.002)。过表达Kindlin-2的GBC-SD在12小时和24小时的伤口愈合率高于对照组((42.9±2.2)%比(29.7±1.7)%,t=4.690,P=0.009;(65.0±2.4)%比(40.4±2.0)%,t=7.945,P=0.001)。过表达Kindlin-2的SGC-996在12小时和24小时的伤口愈合率也高于对照组((32.9±1.3)%比(24.1±1.5)%,t=4.518,P=0.011;(51.3±1.1)%比(39.2±1.1)%,t=8.001,P=0.001)。过表达Kindlin-2可诱导胆囊癌细胞发生EMT,表现为N-钙黏蛋白、波形蛋白表达上调,E-钙黏蛋白表达下调。Kindlin-2在胆囊癌组织中表达上调,其可能通过部分诱导上皮-间质转化促进胆囊癌细胞的恶性表型。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验