Fubo Wang1, Wei Zhang1, Zijian Song1, Maoyu Wang1, Hanxiao Wu1, Yang Yang2, Rui Chen3. 1. Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China. 2. Institute of Clinical Laboratory Medicine, Clinical School of Medical College, Jinling Hospital, Nanjing University, Nanjing, China. yangyang198710@hotmail.com. 3. Department of Urology, Shanghai Changhai Hospital, Second Military Medical University, Shanghai, China. drchenrui@foxmail.com.
Abstract
BACKGROUND: To identify novel miRNAs implicated in prostate cancer metastasis. METHODS: Sixty-five prostate cancer tissues and paired pan-cancer tissues were sequenced. Novel miRNAs were re-analyzed by MIREAP program. Biological functions of miR-N5 were transwell experiment and colony formation. Target genes of miR-N5 were analyzed by bioinformatic analysis. Downstream of target gene was analyzed by The Cancer Genome Atlas (TCGA) and Memorial Sloan Kettering Cancer Center (MSKCC) databases and confirmed by CHIP experiment. RESULTS: We identified a novel miRNA-miR-N5, which was downregulated in PCa cells, PCa tissue, and in the serum of patients with PCa. Knockout of miR-N5 enhanced migration and invasiveness in vitro. miR-N5 specified targeted CREBBP 3'-UTR and inhibited CREBBP expression, which mediated H3K56 acetylation at the promoter of EGFR, β-catenin and CDH1. CONCLUSION: This study may shed the light on miR-N5 which influences metastasis via histone acetylation.
BACKGROUND: To identify novel miRNAs implicated in prostate cancer metastasis. METHODS: Sixty-five prostate cancer tissues and paired pan-cancer tissues were sequenced. Novel miRNAs were re-analyzed by MIREAP program. Biological functions of miR-N5 were transwell experiment and colony formation. Target genes of miR-N5 were analyzed by bioinformatic analysis. Downstream of target gene was analyzed by The Cancer Genome Atlas (TCGA) and Memorial Sloan Kettering Cancer Center (MSKCC) databases and confirmed by CHIP experiment. RESULTS: We identified a novel miRNA-miR-N5, which was downregulated in PCa cells, PCa tissue, and in the serum of patients with PCa. Knockout of miR-N5 enhanced migration and invasiveness in vitro. miR-N5 specified targeted CREBBP 3'-UTR and inhibited CREBBP expression, which mediated H3K56 acetylation at the promoter of EGFR, β-catenin and CDH1. CONCLUSION: This study may shed the light on miR-N5 which influences metastasis via histone acetylation.
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