Small nucleolar RNA host gene 6 (SNHG6) regulates diverse biological processes in cancers. Potential function of SNHG6 in human colon and rectal adenocarcinoma (CRC) was evaluated. Quantitative real-time polymerase chain reaction, MTT assays, Colony formation assays, Transwell assay, Western Blotting and Luciferase reporter assays were performed to measure the biological functions and potential molecular mechanisms of SNHG6 in CRC. SNHG6 was over-expressed in CRC, and high expression of s SNHG6 were associated with short survival times. We then identified miR-101-3p as an inhibitory target of SNHG6. Knockdown of SNHG6 significantly decreased miR-101-3p expression. Moreover, silenced SNHG6 obviously inhibited CRC cell growth, weakened cell invasion capacity and blocked the Wnt/β-catenin signaling pathway. SNHG6 could regulate the progression of CRC via modulating the expression levels of miR-101-3p and the activity of Wnt/β-catenin signaling.

中文翻译：

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SNHG 6通过miR-101-3p和Wnt /β-catenin信号通路促进结肠癌和直肠腺癌的进展

小核仁RNA宿主基因6（SNHG6）调节癌症中的多种生物过程。评估了SNHG6在人结肠和直肠腺癌（CRC）中的潜在功能。进行实时定量聚合酶链反应，MTT测定，菌落形成测定，Transwell测定，蛋白质印迹和荧光素酶报告基因测定，以测量SNHG6在CRC中的生物学功能和潜在的分子机制。SNHG6在CRC中过表达，而s SNHG6的高表达与较短的生存时间有关。然后，我们将miR-101-3p鉴定为SNHG6的抑制靶标。击倒SNHG6大大降低了miR-101-3p表达。此外，沉默的SNHG6明显抑制了CRC细胞的生长，削弱了细胞的侵袭能力，并阻断了Wnt /β-catenin信号通路。