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C/EBPβ 通过促进膀胱癌特异性 lncRNA UCA1 的转录来促进人膀胱癌细胞的活力。

C/EBPβ promotes the viability of human bladder cancer cell by contributing to the transcription of bladder cancer specific lncRNA UCA1.

机构信息

Department of Clinical Laboratory, Peking University First Hospital, Beijing, 100034, China.

Department of Central Laboratory, Peking University Shougang Hospital, Beijing, 100144, China.

出版信息

Biochem Biophys Res Commun. 2018 Nov 30;506(3):674-679. doi: 10.1016/j.bbrc.2018.10.152. Epub 2018 Oct 28.

DOI:10.1016/j.bbrc.2018.10.152
PMID:30376994
Abstract

Urothelial Carcinoma Antigen 1 (UCA1) is a cell and tissue specific long non-coding RNA (lncRNA) associated with the tumorigenesis and invasion of bladder cancer. However, the mechanism driving the over-transcription of UCA1 in bladder cancer cells remains unclear. It has been reported that C/EBPβ has a significant role of regulation in tumorigenesis. Here we report that the expression of UCA1 was dramatically inhibited in 5637 cells with C/EBPβ down-regulation. Additionally, the function tests indicated that C/EBPβ could promote 5637 cells growth and colony formation by inducing the expression level of UCA1. These data suggest that C/EBPβ was involved in transcriptional regulation of UCA1 and contributed substantially to its high expression and proliferation promoting in bladder cancer cells.

摘要

尿路上皮癌相关抗原 1(UCA1)是一种与膀胱癌的发生和侵袭相关的细胞和组织特异性长链非编码 RNA(lncRNA)。然而,驱动膀胱癌细胞中 UCA1 过度转录的机制尚不清楚。据报道,C/EBPβ 在肿瘤发生中具有重要的调节作用。在这里,我们报告说,在下调 C/EBPβ 的 5637 细胞中,UCA1 的表达明显受到抑制。此外,功能测试表明,C/EBPβ 可以通过诱导 UCA1 的表达水平来促进 5637 细胞的生长和集落形成。这些数据表明,C/EBPβ 参与了 UCA1 的转录调控,并在膀胱癌细胞中高表达和促进增殖方面发挥了重要作用。

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