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微小RNA-342-5p和miR-608通过靶向NAA10抑制结肠癌肿瘤发生。

microRNA-342-5p and miR-608 inhibit colon cancer tumorigenesis by targeting NAA10.

作者信息

Yang Hongju, Li Qian, Niu Jie, Li Bai, Jiang Dejun, Wan Zhihua, Yang Qingmei, Jiang Fei, Wei Ping, Bai Song

机构信息

The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.

Human Genetics Center of Yunnan University, Kunming, Yunnan, China.

出版信息

Oncotarget. 2016 Jan 19;7(3):2709-20. doi: 10.18632/oncotarget.6458.

DOI:10.18632/oncotarget.6458
PMID:26646451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4823066/
Abstract

miRNAs have been shown to play pivotal roles in the establishment and progression of colon cancer, but their underlying mechanisms are not fully understood. N-acetyltransferase NAA10 participates in many cellular processes, including tumorigenesis. Here we showed that miR-342-5p and miR-608 suppressed the tumorigenesis of colon cancer cells in vitro and in vivo by targeting NAA10 mRNA for degradation. Overexpression of miR-342-5p or miR-608 decreased NAA10 mRNA and protein levels and thereby suppressed cell proliferation, migration, and cell-cycle progression, as well as promoted apoptosis in SW480 and SW620 cells. More importantly, miR-342-5p and miR-608 significantly decreased the tumorigenic capacity of SW480 and SW620 cells in a mouse xenograft model. We also observed an inverse correlation between the expression of NAA10 and that of both miRNAs. Our results implicate miR-342-5p and miR-608 in colon cancer development and unveil the underlying mechanism of this phenomenon, which involves NAA10.

摘要

微小RNA（miRNAs）已被证明在结肠癌的发生和发展中起关键作用，但其潜在机制尚未完全阐明。N-乙酰转移酶NAA10参与包括肿瘤发生在内的许多细胞过程。在此，我们表明miR-342-5p和miR-608通过靶向NAA10 mRNA进行降解，在体外和体内抑制结肠癌细胞的肿瘤发生。miR-342-5p或miR-608的过表达降低了NAA10 mRNA和蛋白质水平，从而抑制了SW480和SW620细胞的增殖、迁移和细胞周期进程，并促进了细胞凋亡。更重要的是，在小鼠异种移植模型中，miR-342-5p和miR-608显著降低了SW480和SW620细胞的致瘤能力。我们还观察到NAA10的表达与这两种miRNA的表达呈负相关。我们的结果表明miR-342-5p和miR-608参与结肠癌的发展，并揭示了这一现象的潜在机制，其中涉及NAA10。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/ab3f7d7063f2/oncotarget-07-2709-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/0dd63f68edaf/oncotarget-07-2709-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/8e0d3ecb549d/oncotarget-07-2709-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/6f94be997252/oncotarget-07-2709-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/7d4ccc8d61ab/oncotarget-07-2709-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/0329a1713b5b/oncotarget-07-2709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/4c5c3988a46d/oncotarget-07-2709-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/ab3f7d7063f2/oncotarget-07-2709-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/0dd63f68edaf/oncotarget-07-2709-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/8e0d3ecb549d/oncotarget-07-2709-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/6f94be997252/oncotarget-07-2709-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/7d4ccc8d61ab/oncotarget-07-2709-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/0329a1713b5b/oncotarget-07-2709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/4c5c3988a46d/oncotarget-07-2709-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c619/4823066/ab3f7d7063f2/oncotarget-07-2709-g007.jpg

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