ERH基因调控5637和T24膀胱癌细胞的迁移和侵袭

2019年3月，江苏省徐州市中心医院泌尿外科；苏州大学第三附属医院泌尿外科(Department of Urology, Xuzhou Central Hospital, Jiangsu Xuzhou Jiefang South Road, ****99, Jiangsu, China；Department of Urology, The third affiliated hospital of Soochow University,No. 185, Juqian Street, Changzhou City, Jiangsu Province, China) Conghui Han老师研究团队在《BMC CANCER》上发表论文：

“The ERH gene regulates migration and invasion in 5637 and T24 bladder cancer cells”

“ERH基因调控5637和T24膀胱癌细胞的迁移和侵袭”

Abstract：

Background: This study aimed to determine whether the enhancer of the rudimentary homolog (ERH) gene regulates cell migration and invasion in human bladder urothelial carcinoma (BUC) T24 cells and the underlying mechanism.

Methods: First, we knocked down ERH in BUC T24 and 5637 cells by shRNA and then used wound healing cell scratch migration assays, transwell cell migration assays, transwell cell invasion chamber experiments and nude mouse tail vein transfer assays to determine the migration and invasion ability after ERH was knocked down. Moreover, we used gene expression profiling chip analysis and further functional experiments to explore the possible mechanism through which ERH knockdown downregulated metastasis ability in T24 cells.

Results: Wound healing cell scratch migration assays, transwell cell migration assays, transwell cell invasion chamber experiments and nude mouse tail vein transfer assays all showed that the metastasis ability was significantly inhibited in human BUC T24 and 5637 cells with ERH knockdown. A gene expression profiling chip analysis in T24 cells showed that the MYC gene may be an important downstream target of the ERH gene, and the functional experiments showed that MYC is a functional target of ERH in BUC T24 cells.

Conclusion: ERH knockdown could inhibit the metastasis of BUC T24 cells in vitro and in vivo. This study further explored the mechanism of the ERH gene in the metastasis of the T24 human bladder cancer cell line and found that ERH may regulate MYC gene expression. The results of this research provide a basis for the clinical application of ERH as a potential target for BUC treatment.

摘要：

背景

本研究旨在探讨ERH基因增强子是否调控人膀胱尿路上皮癌(BUC) T24细胞的迁移和侵袭及其机制。

方法

首先，研究人员通过shRNA敲除BUC T24和5637细胞中的ERH，然后通过伤口愈合细胞划痕迁移实验、transwell细胞迁移实验、transwell细胞侵袭室实验和裸鼠尾静脉移植实验来测定ERH敲除后的迁移和侵袭能力。此外，研究人员通过基因表达谱芯片分析和进一步的功能实验，探讨ERH敲低下调T24细胞转移能力的可能机制。

结果

伤口愈合细胞划痕迁移实验、transwell细胞迁移实验、transwell细胞侵袭室实验和裸鼠尾静脉转移实验均表明，ERH敲低的人BUC T24和5637细胞的转移能力明显受到抑制。T24细胞基因表达谱芯片分析显示MYC基因可能是ERH基因的重要下游靶点，功能实验显示MYC在BUC T24细胞中是ERH的功能靶点。

结论

ERH敲低可抑制BUC T24细胞的体内外转移。本研究进一步探讨了ERH基因在T24人膀胱癌细胞系转移中的作用机制，发现ERH可能调控MYC基因的表达。本研究结果为ERH作为治疗BUC的潜在靶点的临床应用提供了依据。

该论文中，膀胱癌细胞株5637和T24细胞的体外培养是使用Ausbian特级胎牛血清完成的。欲了解或购买Ausbian特级胎牛血清可以联系北京缔一生物400-166-8600.