Department of Hepatobiliary Surgery, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, Chongqing, China.
J Exp Clin Cancer Res. 2014 Jun 30;33(1):55. doi: 10.1186/1756-9966-33-55.
To understand the involvement of structural maintenance of chromosome 4 (SMC4) in the development and progression of hepatocellular carcinoma (HCC).
Real-time quantitative PCR and Western Blotting were applied to measure the expression of SMC4 in HCC samples and cell lines. The tumor-promoting effect of SMC4 was determined by WST-1, soft agar colony formation, cell motility and invasion assays. The SMC4 target signal pathway was identified by luciferase reporter and real-time quantitative PCR assays.
The upregulation of SMC4 was frequently detected in HCC samples and cell lines. Functional assays demonstrated that SMC4 could effectively promote tumor cell growth rate, colony formation in soft agar, wound-healing and invasion. Further studies showed that increased miR-219 levels caused a significant decrease in the SMC4 expression, and SMC4 inhibitor downregulated JAK2/Stat3 expression at both the mRNA and protein levels.
Our findings provide new insight into SMC4 function and the mechanisms of growth and invasion of HCC.
为了了解染色体 4 结构维持蛋白（SMC4）在肝细胞癌（HCC）发生和发展中的作用。
实时定量 PCR 和 Western Blotting 用于检测 HCC 样本和细胞系中 SMC4 的表达。通过 WST-1、软琼脂集落形成、细胞迁移和侵袭实验测定 SMC4 的促瘤作用。通过荧光素酶报告和实时定量 PCR 实验鉴定 SMC4 的靶信号通路。
SMC4 在 HCC 样本和细胞系中常被上调。功能分析表明，SMC4 可有效促进肿瘤细胞的生长速度、软琼脂中的集落形成、伤口愈合和侵袭。进一步的研究表明，miR-219 水平的升高导致 SMC4 表达显著降低，SMC4 抑制剂下调 JAK2/Stat3 的表达水平在 mRNA 和蛋白水平上。
我们的研究结果为 SMC4 的功能以及 HCC 生长和侵袭的机制提供了新的见解。
