Recently, substantial evidence has demonstrated that long non-coding RNAs (lncRNAs) play critical roles in multiple cancers including colorectal cancer (CRC). Utilizing publicly available lncRNA-expression-profiling data from the Gene Expression Omnibus (GEO) dataset GSE21510, we screened SNHG17 as a new candidate lncRNA associated with CRC development and progression. We further demonstrated that SNHG17 was upregulated in CRC tissues, and that its overexpression was significantly correlated with tumor size, TNM stage, and lymph node metastasis in CRC patients. Moreover, SNHG17 knockdown significantly inhibited the proliferation of CRC cells, and induced cell cycle G1/G0 phase arrest and cell apoptosis. Consistent with these findings, SNHG17 silencing inhibited tumor growth in vivo. Mechanistic studies revealed the capability of lncRNA SNHG17 to epigenetically suppress P57 by binding to enhancer of zeste homolog 2 (a key component of polycomb repressive complex 2) in CRC cells, and quantitative real-time polymerase chain reaction assays demonstrated that SNHG17 expression levels were inversely correlated with those of P57 in CRC tissues. Furthermore, rescue experiments confirmed that SNHG17 exerted oncogenic functions partly through regulating P57 expression. These findings represent the first reporting of the roles and mechanisms associated with SNHG17 in CRC progression, highlighting SNHG17 as a potential therapeutic target for CRC patients.

中文翻译：

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长的非编码RNA SNHG17是不利的预后因素，并通过表观遗传沉默P57促进结直肠癌的细胞增殖

最近，大量证据表明，长的非编码RNA（lncRNA）在包括结直肠癌（CRC）在内的多种癌症中起着至关重要的作用。利用来自基因表达综合（GEO）数据集GSE21510的可公开获得的lncRNA表达谱数据，我们筛选了SNHG17作为与CRC发育和进展相关的新候选lncRNA。我们进一步证明SNHG17在CRC组织中上调，并且其过表达与CRC患者的肿瘤大小，TNM分期和淋巴结转移显着相关。此外，SNHG17基因敲低显着抑制CRC细胞的增殖，并诱导细胞周期G1 / G0期阻滞和细胞凋亡。与这些发现一致的是，SNHG17沉默抑制了体内肿瘤的生长。机理研究表明，lncRNA SNHG17通过与CRC细胞中zeste同源物2（多梳抑制复合物2的关键成分）的增强子结合而表观遗传抑制P57的能力，实时定量聚合酶链反应分析表明SNHG17的表达水平与之相反与CRC组织中的P57相关。此外，救援实验证实SNHG17部分通过调节P57表达发挥致癌作用。这些发现代表了SNHG17在CRC进展中的作用和机制的首次报道，突显了SNHG17作为CRC患者的潜在治疗靶点。