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EZH2通过EMT促进食道状细胞癌的恶性生物行为
Yuying Jing1,2, Kaige Yang3,4, Yiting Cheng3,4
1Department of Pathology, School of Medicine, Shihezi University, Shihezi 832002. 623199820@qq.com.
概括
增强器的zeste同源2 (EZH2) 促进食道状细胞癌 (ESCC) 的进展通过介导上皮层-介质细胞过渡 (EMT). 高EZH2表达与ESCC患者的预后不佳相关,这表明EZH2是潜在的治疗点.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 食道状细胞癌 (ESCC) 呈现出复杂的致病学和不良的患者结果.
- 表皮-介质细胞过渡 (EMT) 越来越多地被认为是它在瘤启动和进展中的作用.
- 在各种癌症中观察到Enhancer of zeste同源2 (EZH2) 的异常表达,可能与EMT有关.
研究的目的:
- 调查EZH2表达及其与ESCC中EMT标记物的相关性.
- 评估EZH2淘汰对ESCC细胞增殖,入侵和迁移的影响.
- 阐明EZH2对ESCC恶性行为的贡献.
主要方法:
- 生物信息学分析评估了ESCC中的EZH2表达.
- 在ESCC细胞系中使用小干扰RNA击败EZH2 (EC109,EC9706).
- 细胞增殖,入侵和迁移通过CCK-8,伤口愈合和Transwell测定进行了测量.
- 蛋白质和mRNA水平的EZH2,E-cadherin (E-cad) 和维丁 (Vim) 通过西方涂抹和RT-qPCR进行了分析.
- 免疫组织化学 (IHC) 染色在ESCC组织和相邻的正常组织上进行,以将EZH2,E-cad和Vim表达与临床病理特征和预后相关联.
主要成果:
- 在ESCC中,EZH2的表达很高,与更差的预后相关 (P<0.001).
- 抑制EZH2显著抑制ESCC细胞的增殖,入侵和迁移 (P<0.001).
- 在蛋白质和mRNA水平上,EZH2沉默导致维丁 (Vim) 减少和E-cadherin (E-cad) 表达增加 (P<0.05).
- 与正常组织相比,IHC在ESCC组织中证实了较高的EZH2和Vim和较低的E-cad表达.
- 低EZH2和Vim表达和高E-cad表达与更长的生存时间相关 (P<0.05).
结论:
- 通过调解EMT,EZH2促进ESCC中的恶性生物行为.
- 升高的EZH2表达是ESCC患者预后不佳的重要指标.
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