Wang Huishan, Wang Li, Tang Lingyu, Luo Jing, Ji Hao, Zhang Wen, Zhou Jian, Li Quanpeng, Miao Lin
Nanjing Medical University, 101 Longmian Avenue, Jiangning District, Nanjing 211166, Jiangsu Province, China.
Taizhou hospital of traditional Chinese medicine, 86 Jichuandong Road, Hailing District, Taizhou 225300, Jiangsu Province, China.
J Cancer. 2020 Mar 4;11(10):3002-3012. doi: 10.7150/jca.40592. eCollection 2020.
Cholangiocarcinoma (CCA) development is an extremely complex process with alterations occurring in numerous genes. SNHG6, a validated lncRNA, has been reported to regulate the expression of multiple tumor-related genes in hepatocellular carcinoma, colorectal cancer and breast cancer. Here, we elucidated the function and possible molecular mechanisms of SNHG6 in human CCA cells. Our results proved that the expression SNHG6 was upregulated in CCA tissues and cell lines. Ectopic expression of SNHG6 promoted cell proliferation, cell cycle progression, migration, and angiogenesis in CCA cells, whereas knockdown of SNHG6 repressed these cellular processes. Further mechanistic studies revealed that SNHG6 could compete with the transcription factor E2F8 to bind with miR-101-3p, thus affecting E2F8 expression. Taken together, these results provided a comprehensive analysis of the role of SNHG6 in CCA cells and offered important clues to understand the key roles of competing endogenous RNA (ceRNA) mechanisms in human cholangiocarcinoma.
胆管癌(CCA)的发生是一个极其复杂的过程,众多基因会发生改变。SNHG6是一种经过验证的长链非编码RNA(lncRNA),据报道它可调节肝癌、结直肠癌和乳腺癌中多个肿瘤相关基因的表达。在此,我们阐明了SNHG6在人CCA细胞中的功能及可能的分子机制。我们的结果证明,SNHG6在CCA组织和细胞系中的表达上调。SNHG6的异位表达促进了CCA细胞的增殖、细胞周期进程、迁移和血管生成,而敲低SNHG6则抑制了这些细胞过程。进一步的机制研究表明,SNHG6可以与转录因子E2F8竞争结合miR-101-3p,从而影响E2F8的表达。综上所述,这些结果对SNHG6在CCA细胞中的作用进行了全面分析,并为理解竞争性内源RNA(ceRNA)机制在人胆管癌中的关键作用提供了重要线索。