ERH基因調(diào)控5637和T24膀胱癌細(xì)胞的遷移和侵襲

2019年3月，江蘇省徐州市中心醫(yī)院泌尿外科；蘇州大學(xué)第三附屬醫(yī)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老師研究團(tuán)隊(duì)在《BMC CANCER》上發(fā)表論文：

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

“ERH基因調(diào)控5637和T24膀胱癌細(xì)胞的遷移和侵襲”

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

本研究旨在探討ERH基因增強(qiáng)子是否調(diào)控人膀胱尿路上皮癌(BUC) T24細(xì)胞的遷移和侵襲及其機(jī)制。

方法

首先，研究人員通過(guò)shRNA敲除BUC T24和5637細(xì)胞中的ERH，然后通過(guò)傷口愈合細(xì)胞劃痕遷移實(shí)驗(yàn)、transwell細(xì)胞遷移實(shí)驗(yàn)、transwell細(xì)胞侵襲室實(shí)驗(yàn)和裸鼠尾靜脈移植實(shí)驗(yàn)來(lái)測(cè)定ERH敲除后的遷移和侵襲能力。此外，研究人員通過(guò)基因表達(dá)譜芯片分析和進(jìn)一步的功能實(shí)驗(yàn)，探討ERH敲低下調(diào)T24細(xì)胞轉(zhuǎn)移能力的可能機(jī)制。

結(jié)果

傷口愈合細(xì)胞劃痕遷移實(shí)驗(yàn)、transwell細(xì)胞遷移實(shí)驗(yàn)、transwell細(xì)胞侵襲室實(shí)驗(yàn)和裸鼠尾靜脈轉(zhuǎn)移實(shí)驗(yàn)均表明，ERH敲低的人BUC T24和5637細(xì)胞的轉(zhuǎn)移能力明顯受到抑制。T24細(xì)胞基因表達(dá)譜芯片分析顯示MYC基因可能是ERH基因的重要下游靶點(diǎn)，功能實(shí)驗(yàn)顯示MYC在BUC T24細(xì)胞中是ERH的功能靶點(diǎn)。

結(jié)論

ERH敲低可抑制BUC T24細(xì)胞的體內(nèi)外轉(zhuǎn)移。本研究進(jìn)一步探討了ERH基因在T24人膀胱癌細(xì)胞系轉(zhuǎn)移中的作用機(jī)制，發(fā)現(xiàn)ERH可能調(diào)控MYC基因的表達(dá)。本研究結(jié)果為ERH作為治療BUC的潛在靶點(diǎn)的臨床應(yīng)用提供了依據(jù)。

該論文中，膀胱癌細(xì)胞株5637和T24細(xì)胞的體外培養(yǎng)是使用Ausbian特級(jí)胎牛血清完成的。欲了解或購(gòu)買(mǎi)Ausbian特級(jí)胎牛血清可以聯(lián)系北京締一生物400-166-8600.