| 何含,刘群,钟庆,等.芬太尼通过 ILF3-AS1/miR-132对卵巢癌细胞生长和转移的影响[J].安徽医药,2022,26(4):765-769. |
| 芬太尼通过 ILF3-AS1/miR-132对卵巢癌细胞生长和转移的影响 |
| Effects of fentanyl on ovarian cancer cell growth and metastasis via ILF3-AS1/miR-132 |
| |
| DOI：10.3969/j.issn.1009-6469.2022.04.028 |
| 中文关键词: 芬太尼 白细胞介素增强结合因子 3反义 RNA1 微小 RNA-132 卵巢癌 |
| 英文关键词: Fentanyl Interleukin enhancer binding factor 3 antisense RNA1 microRNA-132 Ovarian cancer |
| 基金项目: |
|
| 摘要点击次数: 1091 |
| 全文下载次数: 317 |
| 中文摘要: |
| 目的探讨芬太尼对卵巢癌细胞生长和转移的影响及分子机制。方法 2018年 8月至 2019年 10月，体外培养卵巢癌细胞 A2780，用浓度分别为 0、0.5、5、50、500 ng/mL的芬太尼处理，作为不同浓度芬太尼处理组。将过表达的白细胞介素增强结合因子 3反义 RNA1(ILF3-AS1)(pcDNA3.1-ILF3-AS1、对照 pcDNA3.1)、抑制微小 RNA(miRNA/miR)-132表达(抗 -miR-132、对照 anti-miR-NC)的载体分别转染 A2780细胞，并以 500 ng/mL芬太尼处理，记为芬太尼 500+pcDNA3.1-ILF3-AS1组、芬太尼 500+pcDNA3.1组、芬太尼 500+anti-miR-132组、芬太尼 500+anti-miR-NC组。将 pcDNA3.1、pcDNA3.1-ILF3-AS1、si-NC、si-ILF3AS1转染至 A2780细胞中，记为 pcDNA3.1组、 pcDNA3.1-ILF3-AS1组、 si-NC组、 si-ILF3-AS1组。四甲基偶氮唑盐比色法( MTT)检测细胞存活率；克隆形成实验检测细胞克隆形成数； Transwell检测细胞迁移和侵袭；实时荧光定量 PCR(RT-qPCR)检测 ILF3-AS1和 miR-132的表达水平；荧光素酶报告实验检测 ILF3-AS1和 miR-132的靶向关系。结果与 0 ng/mL芬太尼处理组相比， 5、50、500 ng/mL的芬太尼处理的 A2780中 miR-132表达水平显著升高［( 1.39±0.13)、(1.68±0.17)、(2.34±0.23)比( 1.00± |
| 英文摘要: |
| Objective To investigate the effect and molecular mechanism of fentanyl on the growth and metastasis of ovarian cancer cells.Methods From August 2018 to October 2019, ovarian cancer A2780 cells were cultured in vitro and treated with fentanyl at con centrations of 0, 0.5, 5, 50, and 500 ng/mL, as different fentanyl treatment groups. The interleukin enhancer binding factor 3 antisenseRNA1 (ILF3-AS1) overexpression plasmid (pcDNA3.1-ILF3-AS1, control pcDNA3.1) and microRNA-132 (miR-132) siRNA (anti-miR132, control anti-miR-NC vector) were transfected into A2780 cells and then treated with 500 ng/mL fentanyl, recorded as the fentanyl 500+pcDNA3.1-ILF3-AS1 group, fentanyl 500+pcDNA3.1 group, fentanyl 500+anti-miR-132 group and fentanyl 500+anti-miR-NC group. The pcDNA3.1, pcDNA3.1-ILF3-AS1, si-NC, si-ILF3-AS1 were transfected into A2780 cells and recorded as the pcDNA3.1 group, pcDNA3.1-ILF3-AS1 group, si-NC group and si-ILF3-AS1 group. Cell viability was detected by MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide) assay; clone formation assay was used to detect the number of cell clones; Transwell was used to de tect cell migration and invasion; real-time quantitative PCR (RT-qPCR) was used to detect ILF3-AS1 and miR-132 expression level; the targeting relationship between ILF3-AS1 and miR-132 was detected by luciferase reporter assay.Results Compared with the 0 ng/mL fentanyl-treatment group, the expression level of miR-132 in A2780 cells was significantly increased in the 5, 50, and 500 ng/mL fentan yl treatment groups [(1.39±0.13), (1.68±0.17) , (2.34±0.23) vs (1.00±0.10)]; the cell viability [(86.14±8.25)%, (71.03±7.11)%, (43.26± 4.34)% vs (100.01±10.01)%], the number of colonies formed, the number of migrating and invasive cells was significantly decreased, andthe expression level of ILF3-AS1 was significantly decreased [(0.78±0.08), (0.54±0.05), (0.30±0.03) vs (1.01±0.10)] (P<0.05). Both ILF3-AS1 overexpression and miR-132 inhibition reversed the inhibitory effects of fentanyl on the proliferation, migration, and invasion of A2780 cells. ILF3-AS1 targets the expression of miR-132.Conclusion Fentanyl can inhibit ovarian cancer cell proliferation, migra tion and invasion when the concentration is greater than 5 ng/mL, and the mechanism may be related to ILF3-AS1 and miR-132. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
