MiR-301b promotes the proliferation, mobility, and epithelial-to-mesenchymal transition of bladder cancer cells by targeting EGR1

We investigated the role of miR-301b in the modulation of the proliferation, migration, and invasion of bladder cancer (BLCA) cells. The expression of miR-301b and EGR1 (early growth response gene 1) mRNA were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). A dual-luciferase...

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Published inBiochemistry and cell biology Vol. 95; no. 5; pp. 571 - 577
Main Authors Yan, Lei, Wang, Yan, Liang, Jun, Liu, Zhixin, Sun, Xiaodong, Cai, Kerui
Format Journal Article
LanguageEnglish
Published Canada NRC Research Press 01.10.2017
Canadian Science Publishing NRC Research Press
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Summary:We investigated the role of miR-301b in the modulation of the proliferation, migration, and invasion of bladder cancer (BLCA) cells. The expression of miR-301b and EGR1 (early growth response gene 1) mRNA were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). A dual-luciferase reporter gene system was used to identify the target relationship between miR-301b and EGR1. Cell proliferation, cell cycle, and apoptosis were analyzed by MTT assay, colony-forming assay, and flow cytometry, respectively. Cell motility and invasiveness were assessed by wound healing and Transwell assays. The expression of proteins involved in epithelial-to-mesenchymal transition (EMT) and EGR1 were determined by Western blot. Our results showed that miR-301b was up-regulated while EGR1 was down-regulated in BLCA tissues compared with adjacent normal tissues. The proliferation, migration, and invasiveness of T24 cells (a kind of human BLCA cell) were suppressed by decreasing miR-301b expression or increasing EGR1 expression. In addition, miR-301b promoted EMT signaling by influencing the expression of related proteins. In conclusion, miR-301b promotes the proliferation, migration, and aggressiveness of human BLCA cells by inhibiting the expression of EGR1.
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ISSN:0829-8211
1208-6002
DOI:10.1139/bcb-2016-0232