MiR‐1247‐5p is overexpressed in castration resistant prostate cancer and targets MYCBP2

前列腺癌 小RNA LNCaP公司 癌症研究 荧光素酶 转染 污渍 前列腺 信使核糖核酸 基因表达 下调和上调 基因 生物 癌症 医学 内科学 遗传学
作者
Mauro Scaravilli,Kimmo Porkka,Anniina Brofeldt,Matti Annala,Teuvo L.J. Tammela,Guido Jenster,Matti Nykter,Tapio Visakorpi
出处
期刊:The Prostate [Wiley]
卷期号:75 (8): 798-805 被引量:51
标识
DOI:10.1002/pros.22961
摘要

BACKGROUND Recently, there has been increasing attention on the role of microRNAs (miRNAs) in cancer development. Several expression profiling studies have provided evidence of aberrant expression of miRNAs in prostate cancer and have highlighted the potential use of specific miRNA expression signatures as prognostic or predictive markers. Here we report an expression analysis of miR‐1247–5p, miR‐1249, miR‐1269a, miR‐1271–5p, miR‐1290, miR‐1291, and miR‐1299. METHODS qRT‐PCR was performed to validate the differential expression of miRNAs in clinical samples, and the effect of miR‐1247–5p was studied in prostate cancer cell lines transiently transfected with a miR‐1247–5p mimic. The expression of miR‐1247–5p's putative target MYCBP2 was evaluated by qRT‐PCR and Western blotting, and the interaction of the miRNA with the target gene was assessed using a luciferase assay. RESULTS We found a significant up‐regulation of miR‐1247–5p in castration‐resistant prostate cancer (CRPC) samples compared to non‐malignant prostate. The expression of miR‐1247–5p was subsequently studied in prostate cancer (PC) cell lines where an up‐regulation of miR‐1247–5p was observed in the androgen‐independent PC‐3 model. Target prediction analysis for miR‐1247–5p performed online revealed that MYCBP2 (myc‐binding protein 2) was a high‐scoring potential target. Functional studies in vitro performed using PC‐3 and LNCaP models confirmed the down‐regulation of MYCBP2 at the mRNA and protein levels, and a luciferase assay showed interaction between the miRNA and target gene. CONCLUSION miR‐1247–5p is overexpressed in CRPC and targets MYCBP2. Prostate 75:798–805, 2015 . © 2015 Wiley Periodicals, Inc.

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