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

Bo Jin; Yanbing Gong; Haixia Li; Lili Jiao; Dianqi Xin; Yanqing Gong; Zhisong He; Liqun Zhou; Yaqiong Jin; Xiujuan Wang; Zheng Zhang

doi:10.1016/j.bbrc.2018.10.152

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

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

Authors

Bo Jin¹, Yanbing Gong², Haixia Li¹, Lili Jiao¹, Dianqi Xin³, Yanqing Gong³, Zhisong He³, Liqun Zhou³, Yaqiong Jin⁴, Xiujuan Wang⁵, Zheng Zhang⁶

Affiliations

¹ Department of Clinical Laboratory, Peking University First Hospital, Beijing, 100034, China.
² Department of Central Laboratory, Peking University Shougang Hospital, Beijing, 100144, China.
³ Department of Urology, Peking University First Hospital & Institute of Urology, Peking University, Beijing, 100034, China.
⁴ Biobank for Clinical Data and Samples in Pediatric, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, 100045, China.
⁵ Department of Clinical Laboratory, Shandong Academy of Medical Sciences, Shandong Cancer Hospital Affiliated to Shandong University, Jinan, 250117, Shandong, China.
⁶ Department of Urology, Peking University First Hospital & Institute of Urology, Peking University, Beijing, 100034, China. Electronic address: zhangzheng@pkufh.com.

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

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.

Keywords: Bladder cancer; C/EBPβ; UCA1; lncRNA.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

CCAAT-Enhancer-Binding Protein-beta / metabolism*
Cell Line, Tumor
Cell Proliferation / genetics
Cell Survival / genetics
Gene Expression Regulation, Neoplastic
Humans
Promoter Regions, Genetic / genetics
Protein Binding
RNA, Long Noncoding / genetics*
RNA, Long Noncoding / metabolism
Transcription, Genetic*
Urinary Bladder Neoplasms / genetics*
Urinary Bladder Neoplasms / pathology*

Substances

CCAAT-Enhancer-Binding Protein-beta
RNA, Long Noncoding
UCA1 RNA, human