文章摘要
曹峰,刘敏,赵潇.舒芬太尼调控 miR-1抑制肝癌细胞 MHCC97-H增殖、侵袭和迁移的机制研究[J].安徽医药,2021,25(10):1938-1942.
舒芬太尼调控 miR-1抑制肝癌细胞 MHCC97-H增殖、侵袭和迁移的机制研究
Mechanism of sufentanil inhibiting proliferation, invasion and migration of hepatocellular carcinoma cell line MHCC97-H by regulating miR-1
  
DOI:10.3969/j.issn.1009-6469.2021.10.007
中文关键词: 舒芬太尼  肝肿瘤  微小 RNA-1  人肝癌 MHCC97-H细胞  增殖  侵袭  迁移
英文关键词: Sufentanil  Liver neoplasms  miR-1  Human liver cancer MHCC97-H cells  Proliferation  Invasion  Migration
基金项目:
作者单位
曹峰 北京中医药大学枣庄医院外三科山东枣庄 277800 
刘敏 北京中医药大学枣庄医院 手术室山东枣庄 277800 
赵潇 枣庄矿业集团中心医院手术室山东枣庄 277800 
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中文摘要:
      目的探讨舒芬太尼调控微小 RNA-1(miR-1)表达对人肝癌 MHCC97-H细胞增殖、侵袭和迁移的影响及其机制。方法本研究起止时间为 2018年 3月至 2019年 9月,采用细胞计数试剂盒(CCK-8)实验检测不同浓度的舒芬太尼对人肝癌 MHCC97-H细胞活力的影响, qRT-PCR检测舒芬太尼对 MHCC97-H细胞中 miR-1表达的影响;通过脂质体转染法将 miR-1抑制剂(inhibitor)及阴性对照转染至 MHCC97-H细胞,实验分为 Control组、舒芬太尼( Sufentanil)组、转染对照( Sufentanil+NC)组和转染( Sufentanil+miR-1)组。细胞计数试剂盒(CCK-8)实验检测各组 MHCC97-H细胞增殖能力, Transwell实验检测各组 MHCC97-H细胞侵袭能力,划痕实验检测各组 MHCC97-H细胞迁移能力,蛋白质印迹法( Western blotting)检测各组 MHCC97-H细胞中基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶 -9(MMP-9)蛋白表达情况。结果不同浓度的舒芬太尼对肝癌 MHCC97-H细胞活力具有不同程度的抑制作用;与 Control组比, Sufentanil组 MHCC97-H细胞中 miR-1的表达[(1.00±0.09)比( 2.25±0.24)]明显升高( P<0.05),细胞增殖[(0.54±0.05)比(0.34±0.03)]侵袭[(106.24±8.25)个比(51.34±5.02)个]和迁移能力[(37.36±4.01)%比(16.34±1.72)%]降低(P<0.05)MMP-2[(0.33±0.04)比(0.、15±0.02)]和 MMP-9[(0.24±0.02)(0.11±0.01)]的表达下调(P<0.05);与 Sufentanil+NC组比, Sufentanil+,miR-1组 MHCC97-H细胞中 miR-1的表达[(2.20±0.21)比(1比.42±0.15)]明显降低(P<0.05),细胞增殖[(0.32±0.03)比( 0.46±0.04)]、侵袭[(52.36±5.14)个比( 91.16±6.06)个]和迁移能力[( 17.11±1.71)%比( 29.85±3.10)%]升高( P<0.05),MMP-2[(0.15±0.02)比(0.27±0.02)]和 MMP-9[(0.13±0.01)比(0.19±0.02)]的表达上调(P<0.05)。结论舒芬太尼可通过调控 miR-1的表达抑制人肝癌 MHCC97-H细胞的增殖、侵袭和迁移,其机制可能与调控 MMP-2和 MMP-9表达有关。
英文摘要:
      Objective To explore the effect and mechanism of sufentanil on the proliferation, invasion and migration of human hepatocellular carcinoma cell line MHCC97-H by regulating microRNA-1 (miR-1) expression.Methods The start and end time of this research was from March 2018 to September 2019.The effects of different concentrations of sufentanil on the viability of human hepatocellular carcinoma cell line MHCC97-H were determined using the cell counting kit-8 (CCK-8) assay. The effect of sufentanil on the expression of miR-1 in MHCC97-H cells was detected by qRT-PCR. The miR-1 inhibitor and negative control were transfected into MHCC97-H cells using liposome-mediated transfection. There were control group, sufentanil group, sufentanil+NC group and sufentanil+miR-1 group in this study. The proliferation, invasion and migration ability of MHCC97-H cells in each group was detected by CCK-8 assay, Transwell assay, and scratch test, respectively. Western blotting was used to detect the expressions of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) in MHCC97-H cells.Results Different concentrations of sufentanil had different inhibitory effects on the viability of MHCC97-H cells in vitro. Compared with the control group, the expression of miR-1 in MHCC97-H cells in the sufentanil group [(1.00±0.09) vs. (2.25±0.24)] was significantly higher (P<0.05), the cell proliferation [(0.54± 0.05) vs. (0.34±0.03)], invasion [(106.24±8.25) vs. (51.34±5.02)] and migration ability [(37.36±4.01)% vs. (16.34±1.72)%] decreased (P <0.05), and MMP-2 [(0.33±0.04) vs. (0.15±0.02)] and MMP-9 [(0.24±0.02) vs. (0.11±0.01)] expressions were down-regulated (P<0.05). Compared with sufentanil+NC group, the expression of miR-1 in MHCC97-H cells in the sufentanil+miR-1 group [(2.20±0.21) vs. (1.42±0.15)] was significantly reduced (P<0.05), cell proliferation [(0.32±0.03) vs. (0.46±0.04)], invasion [ (52.36±5.14) vs. (91.16± 6.06)] and migration ability [(17.11±1.71)% vs. (29.85±3.10)%] increased (P<0.05), and MMP-2 [(0.15±0.02) vs. (0.27±0.02)] and MMP-9 [(0.13±0.01) vs. (0.19±0.02)] expressions were up-regulated (P<0.05).Conclusion Sufentanil can inhibit the proliferation, invasion and migration of human hepatocellular carcinoma cell line MHCC97-H by regulating the expression of miR-1, whose mechanism may be related to the regulation of MMP-2 and MMP-9 expressions.
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