| 引用本文: |
屈健,郑颖怀,杨炼,罗雪娥,唐宏英.长链非编码RNA SNHG10对胰腺癌细胞的迁移及侵袭的影响[J].湖南中医药大学学报,2020,40(8):945-950[点击复制] |
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| 长链非编码RNA SNHG10对胰腺癌细胞的迁移及侵袭的影响 |
| 屈健,郑颖怀,杨炼,罗雪娥,唐宏英 |
| (湖南省人民医院肝胆外科, 湖南 长沙 410011;中南大学湘雅二医院普外科, 湖南 长沙 410011) |
| 摘要: |
| 目的 分析长链非编码RNA（long non-coding RNA,lncRNA）小核仁RNA宿主基因10（small nucleolar RNA host gene 10,SNHG10）在胰腺癌（pancreatic cancer,PC）细胞中的表达水平，并观察其对细胞迁移及侵袭能力的影响。方法 采用荧光定量PCR（qRT-PCR）检测5株PC细胞（AsPC-1、Capan-1、CFPAC-1、PANC-1和PaCa-2）和正常胰腺导管上皮细胞（HPDE）中SNHG10的表达特征。采用pcDNA3.1(+)-SNHG10载体过表达SNHG10，以pcDNA3.1(+)载体为对照；采用shRNA-SNHG10载体干扰SNHG10表达，以shRNA-control载体为对照。采用细胞划痕和Transwell侵袭试验观察过表达和干扰SNHG10后AsPC-1和PANC-1细胞迁移及侵袭能力的变化。结果 SNHG10在AsPC-1、Capan-1、CFPAC-1、PANC-1和PaCa-2细胞中的表达水平均显著高于HPDE细胞（P<0.05），并以AsPC-1和PANC-1细胞的表达水平为最高（P<0.05）。转染pcDNA3.1(+)-SNHG10载体可显著提高AsPC-1和PANC-1细胞中SNHG10的表达水平（P<0.05），而转染shRNA-SNHG10载体显著抑制AsPC-1和PANC-1细胞中SNHG10的表达水平（P<0.05）。转染shRNA-SNHG10载体可显著促进AsPC-1和PANC-1细胞的迁移及侵袭能力（P<0.05），而转染shRNA-NHG10载体显著抑制AsPC-1和PANC-1细胞的迁移及侵袭能力（P<0.05）。结论 SNHG10在PC细胞中表达上调。过表达SNHG10可促进PC细胞的迁移及侵袭能力，而干扰SNHG10可抑制PC细胞的迁移及侵袭能力。 |
| 关键词: SNHG10 胰腺癌 长链非编码RNA 迁移 侵袭 |
| DOI：10.3969/j.issn.1674-070X.2020.08.008 |
| 投稿时间：2019-07-30 |
| 基金项目:湖南省人民医院青年博士基金项目（BSJJ201808）。 |
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| Effects of Long Non-Coding RNA SNHG10 on Migration and Invasion of Pancreatic Cancer Cells |
| QU Jian,ZHENG Yinghuai,YANG Lian,LUO Xue'e,TANG Hongying |
| (Department of Hepatobiliary Surgery, Hunan Provincial People's Hospital, Changsha, Hunan 410011, China;Department of General Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, China) |
| Abstract: |
| Objective To analyze the expression levels of long non-coding RNA (lncRNA) small nucleolar RNA host gene 10 (SNHG10) in pancreatic cancer (PC) cells, and to investigate its effects on the migratory and invasive abilities of PC cells. Methods The expression patterns of SNHG10 in 5 types of PC cells (AsPC-1, Capan-1, CFPAC-1, PANC-1 and PaCa-2) and a normal pancreatic ductal epithelial cell (HPDE) was observed by quantitative real-time PCR (qRT-PCR). The shRNA3.1 (+)-SNHG10 vector was used to enforce SNHG10 expression, and the pcDNA3.1 (+) vector was served as a negative control. The shRNA-SNHG10 vector was used to silence SNHG10 expression, and the shRNA-control vector was served as a negative control. The migratory and invasive abilities of AsPC-1 and PANC-1 cells after knockdown and overexpression of SNHG10 were evaluated by cell scratch and Transwell invasion assays, respectively. Results The expression levels of SNHG10 in the AsPC-1, Capan-1, CFPAC-1, PANC-1 and PaCa-2 cells were significantly higher than that in the HPDE cells (P<0.05), and the SNHG10 expression of the AsPC-1 and PANC-1 cells was the highest (P<0.05). Transfection of pcDNA3.1 (+)-SNHG10 vector significantly increased the expression levels of SNHG10 in the AsPC-1 and PANC-1 cells (P<0.05), whereas transfection of shRNA-SNHG10 vector markedly inhibited the expression levels of SNHG10 in theAsPC-1 and PANC-1 cells (P<0.05). Transfection of shRNA-SNHG10 vector significantly promoted the migratory and invasive abilities of theAsPC-1 and PANC-1 cells (P<0.05), while transfection of shRNA-SNHG10 vector markedly inhibited the migratory and invasive abilities of theAsPC-1 and PANC-1 cells (P<0.05). Conclusion SNHG10 expression is upregulated in PC cells. Overexpression of SNHG10 promotes the migratory and invasive abilities of PC cells, while knockdown of SNHG10 inhibits the migratory and invasive abilities of PC cells. |
| Key words: SNHG10 pancreatic carcinoma long non-coding RNA migration invasion |
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