The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal cancer.
The long non-coding RNA SNHG3 functions as a competing endogenous RNA to promote malignant development of colorectal cancer.
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DOI：
10.3892/or.2017.5837
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发表时间：
2017-09
期刊：
影响因子：
4.2
通讯作者：
Yuan X
中科院分区：
文献类型：
--
作者：
Huang W;Tian Y;Dong S;Cha Y;Li J;Guo X;Yuan X
越来越多的证据表明，异常表达的长非编码转录本参与结直肠癌（CRC）的发生和发展。小核仁RNA宿主基因3（SNHG 3）是一种新发现的lncRNA，其在结直肠癌发生发展中的生物学功能及临床意义尚不清楚。在本研究中，我们发现SNHG 3的表达在CRC中显著上调，并且通过分析从TCGA数据库获得的数据确定SNHG 3的上调预测CRC患者的不良预后。功能获得和功能丧失试验显示SNHG 3显著促进CRC细胞的细胞增殖。基因集富集分析（Gene Set Enrichment Analysis，GSEA）显示SNHG 3的高表达与c-Myc及其靶基因的表达呈正相关。此外，SNHG 3的异位过表达增加了c-Myc及其靶基因的表达，而SNHG 3的抑制对c-Myc及其靶基因的表达具有相反的作用。机制研究表明，SNHG 3作为竞争性内源性RNA（ceRNA）"海绵" miR-182 - 5p，从而导致c-Myc从miR-182 - 5p释放并调节c-Myc的表达。总之，SNHG 3通过海绵状miR-182 - 5p和上调c-Myc及其靶基因促进CRC进展。
Accumulating evidence has revealed that aberrantly expressed long non-coding transcripts are involved in the development and progression of colorectal cancer (CRC). Small nucleolar RNA host gene 3 (SNHG3) is a newly identified lncRNA, and little is known about its clinical significance and biological functions in the development of CRC. In the present study, we found that the expression of SNHG3 was significantly upregulated in CRC, and upregulation of SNHG3 predicted poor prognosis for patients with CRC as determined through analysis of the data obtained from TCGA database. Gain-of function and loss-of function assays revealed that SNHG3 markedly promoted cellular proliferation of CRC cells. Gene Set Enrichment Analysis (GSEA) suggested that high expression of SNHG3 was positively associated with c-Myc and its targets genes. Furthermore, ectopic overexpression of SNHG3 increased the expression of c-Myc and its target genes, whereas inhibition of SNHG3 had opposite effect on the expression of c-Myc and its targets. Mechanistic investigations demonstrated that SNHG3 functioned as a competing endogenous RNA (ceRNA) to ‘sponge’ miR-182-5p, thus leading to the release of c-Myc from miR-182-5p and modulating the expression of c-Myc. In conclusion, SNHG3 promoted CRC progression via sponging miR-182-5p and upregulating c-Myc and its target genes.
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影响因子：
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作者：
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通讯作者：
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影响因子：
7.5
作者：
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通讯作者：
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