首页|MSC-AS1对宫颈癌细胞生物学行为的影响及其机制

MSC-AS1对宫颈癌细胞生物学行为的影响及其机制

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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。
Effects of MSC-AS1 on the biological behavior of cervical cancer cells and the mechanism
Aim To explore the role and mechanism of long non-coding RNA(lncRNA)MSC-AS1 in the biological behavior of cervical cancer cells.Methods qRT-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 apop-tosis,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.Results Com-pared 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 vec-tor 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).Conclusion Silencing MSC-AS1 may target ATAD2 through miR-520d-3p to inhibit the growth and metastasis of cervical cancer cells,and promote apoptosis.

cervical cancercell biological behaviorMSC-AS1miR-520d-3pATAD2

徐香、耿杨柳

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国药东风总医院妇产科,湖北十堰 442000

宫颈癌 细胞生物行为 MSC-AS1 miR-520d-3p ATAD2

十堰市科技局医药科技发展项目

2022KJ0135

2024

中南医学科学杂志
南华大学

中南医学科学杂志

CSTPCD
影响因子:0.757
ISSN:2095-1116
年,卷(期):2024.52(3)