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 in | Biochemistry and cell biology Vol. 95; no. 5; pp. 571 - 577 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Canada
NRC Research Press
01.10.2017
Canadian Science Publishing NRC Research Press |
Subjects | |
Online Access | Get full text |
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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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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 ObjectType-Correction/Retraction-3 |
ISSN: | 0829-8211 1208-6002 |
DOI: | 10.1139/bcb-2016-0232 |