长链非编码 RNA SNHG11 对结直肠癌增殖的影响

目的 探讨长链非编码 RNA 小核仁 RNA 宿主基因 11 ( small nucleolar RNA host gene 11, SNHG11) 对结直肠癌增殖的影响及分子机制。 方法 人结肠癌细胞 LOVO、 SW480 构建 SNHG11 过表达或 者 SNHG11 干扰细胞株, 检测在结直肠癌细胞株中过表达及干扰 SNHG11 后, 结直肠癌细胞增殖能力、 P50 和 P65 蛋白和 NF-κB 信号通路下游基因的表达情况。 结果 过表达 SNHG11 能促进结直肠癌细胞的增殖, 而抑制 SNHG11 的表达则能明显抑制结直肠癌细胞的增殖。 过表达 SNHG11 后 P65、 P50 的表达及 NF-κB 信号 通路下游与细胞增殖相关基因 c-Myc、 COX2、 CCND1、 VEGFA 水平明显上调; 而敲除 SNHG11 后则显著降低。 SNHG11 通过与 NF-κB 复合体中的 P50 结合, 进而上调 NF-κB 复合体, 激活 NF-κB 信号通路。 结论 长链非 编码 RNA SNHG11 通过激活 NF-κB 信号通路促进结直肠癌细胞的增殖。

Effect of Long Non-Coding RNA SNHG11 on Proliferation of Colorec-tal Cancer

Objective To investigate the effect of long-chain noncoding RNA small nucleolar RNA host gene 11 ( SNHG11) on the proliferation of colorectal cancer and its molecular mechanism. Methods SNHG11 overexpression or knock-down cell lines were constructed in human colon cancer cell lines LoVo and SW480. The proliferation ability of the colorectal cancer cells was assayed after SNHG11 overexpression or knock-down. The expression levels of P50, P65 and NF-κB downstream signaling proteins were detected after overexpression and interference of SNHG11 in colorectal cancer cell lines. Results Overexpression of SNHG11 could promote the proliferation of colorectal cancer cells, while inhibition of SNHG11 expression could significantly inhibit the proliferation of colorectal cancer cells. The expression levels of P65, P50, NF-κB downstream signaling proteins and the expression levels of proliferation-related genes c-myc, COX2, CCND1 and VEGFA were significantly up-regulated after overexpression of SNHG11. However, their expression levels were decreased significantly after knock-out of SNHG11. SNHG11 could up-regulate NF-κB complex and activate NFκB signaling pathway via binding to P50 in the NF-κB complex. Conclusion Long non-coding RNA SNHG11 promotes colorectal cancer cell proliferation by activating NF-κB signaling pathway.