| 徐香,耿杨柳.MSC-AS1对宫颈癌细胞生物学行为的影响及其机制.[J].中南医学科学杂志.,2024,(3):358-363. |
| MSC-AS1对宫颈癌细胞生物学行为的影响及其机制 |
| Effects of MSC-AS1 on the biological behavior of cervical cancer cells and the mechanism |
| 投稿时间：2023-07-21 修订日期：2024-04-15 |
| DOI：10.15972/j.cnki.43-1509/r.2024.03.010 |
| 中文关键词: 宫颈癌 细胞生物行为 MSC-AS1 miR-520d-3p ATAD2 [ |
| 英文关键词:cervical cancer cell biological behavior MSC-AS1 miR-520d-3p ATAD2 |
| 基金项目:十堰市科技局医药科技发展项目(2022KJ0135) |
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| 中文摘要: |
| 目的探索长链非编码RNA(lncRNA)MSC-AS1在宫颈癌细胞生物行为中的作用和机制。 方法qRT-PCR和Western blotting检测MSC-AS1、miR-520d-3p和三磷酸腺苷酶家族蛋白2(ATAD2)在宫颈癌组织和SiHa细胞中的表达。SiHa细胞分为si-NC组、si-MSC-AS1组、vector组、pc3.1-MSC-AS1组、miR-NC组、miR-520d-3p组、si-NC+anti-miR-NC组、si-MSC-AS1+anti-miR-NC组、si-MSC-AS1+anti-miR-520d-3p组。流式细胞术、Transwell实验分别检测细胞凋亡、迁移和侵袭水平的变化。软件预测结合双荧光素酶活性实验分析MSC-AS1、miR-520d-3p、ATAD2之间的靶向调控关系。 结果与癌旁组织比较,宫颈癌组织MSC-AS1、ATAD2表达上调,miR-520d-3p表达下调(P＜0.05)。SiHa细胞凋亡率、miR-520d-3p表达水平在沉默MSC-AS1后si-MSC-AS1组高于si-NC组,过表达MSC-AS1后pc3.1-MSC-AS1组低于vector组；沉默MSC-AS1同时抑制miR-520d-3p后si-NC+anti-miR-NC组＜si-MSC-AS1+anti-miR-520d-3组＜si-MSC-AS1+anti-miR-NC组(P＜0.05)。MSC-AS1靶向miR-520d-3p,且miR-520d-3p靶向ATAD2,miR-520d-3p组SiHa细胞凋亡率高于miR-NC组(P＜0.05)。SiHa细胞ATAD2蛋白的表达、迁移和侵袭细胞数si-MSC-AS1组低于si-NC组,pc3.1-MSC-AS1组高于vector组,miR-520d-3p组低于miR-NC组,si-NC+anti-miR-NC组＞si-MSC-AS1+anti-miR-520d-3p组＞si-MSC-AS1+anti-miR-NC组(P＜0.05)。 结论沉默MSC-AS1可能通过miR-520d-3p靶向ATAD2,抑制宫颈癌细胞的生长和转移,并促进凋亡。 |
| 英文摘要: |
| AimTo explore the role and mechanism of long non-coding RNA (lncRNA) MSC-AS1 in the biological behavior of cervical cancer cells. MethodsqRT-PCR and Western blotting were used to detect the expression of MSC-AS1, miR-520d-3p and ATAD2 in cervical cancer tissues and SiHa cells. SiHa cells were divided into si-NC group, si-MSC-AS1 group, vector group, pc3.1-MSC-AS1 group, miR-NC group, miR-520d-3p group, si-NC+anti-miR-NC group, si-MSC-AS1+anti-miR-NC group, and si-MSC-AS1+anti-miR-520d-3p group. Flow cytometry, and Transwell experiment were used to evaluate the changes of cell apoptosis, and migration and invasion levels, respectively. The targeted regulatory relationships among MSC-ASI , miR-520d -3p, ATAD2 were analyzed by combining starbase software and targetscan software with luciferase activity experiments. ResultsCompared with adjacent tissues, the expression of MSC-AS1 and ATAD2 protein in cervical cancer tissues were upregulated, while miR-520d-3p was downregulated (P＜0.05). After silencing MSC-AS1, the expression of miR-520d-3p and apoptosis rate of SiHa cells were higher in the si-MSC-AS1 group compared with the si-NC group, and lower in the pc3.1-MSC-AS1 group compared with the vector group after overexpression of MSC-AS1. After silencing MSC-AS1 while inhibiting miR-520d-3p, the expression of miR-520d-3p and apoptosis rate of SiHa cells were in an order of si-NC+anti-miR-NC group＜si-MSC-AS1+anti-miR-520d-3p group＜si-MSC-AS1+anti-miR-NC group (P＜0.05). MSC-AS1 targets miR-520d-3p, while miR-520d-3p targets ATAD2, and the apoptosis rate of SiHa cell in miR-520d-3p group were higher than in the miR-NC group (P＜0.05). The ATAD2 protein levels, migration number, invasion number of SiHa cells were lower in the si-MSC-AS1 group than in the si-NC group, higher in the pc3.1-MSC-AS1group than in the vector group, ad lower in the miR-520d-3p group than in the miR-NC group, in an order of si-NC+anti-miR-NC group＞si-MSC-AS1+anti-miR-520d-3p group＞si-MSC-AS1+anti-miR-NC group (P＜0.05). ConclusionSilencing MSC-AS1 may target ATAD2 through miR-520d-3p to inhibit the growth and metastasis of cervical cancer cells, and promote apoptosis. |
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