lncRNA SNHG6调节miR-186-5p/SEPT2轴对乳腺癌细胞上皮间质转化的影响  

Influence of IncRNA SNHG6 on epithelial mesenchymal transition of breast cancer cells by regulating miR-186-5p/SEPT2 axis

作　　者：张暖[1] 王志鹏[1] ZHANG Nuan;WANG Zhipeng(Department of Oncology,Afiliated Hospital of Shandong University of Traditional Chinese Medicine,Jinan,Shandong 250000,China)

机构地区：[1]山东中医药大学附属医院肿瘤内科,山东济南250000

出　　处：《中国优生与遗传杂志》2024年第1期1-8,共8页Chinese Journal of Birth Health & Heredity

摘　　要：目的探讨lncRNA SNHG6通过调节miR-186-5p/SEPT2轴对乳腺癌(BC)细胞上皮间质转化(EMT)的影响。方法qRT-PCR检测BC组织和细胞中SNHG6、miR-186-5p、SEPT2mRNA表达水平,筛选最佳干预细胞系;双萤光素酶报告基因实验验证SNHG6、SEPT2与miR-186-5p靶向调控关系,EdU、CCK-8法测定细胞增殖,流式细胞术检测细胞凋亡,Transwell小室实验检测细胞迁移和侵袭数,Western blot检测SEPT2、E-cadherin、N-cadherin、Vimentin蛋白表达。建立裸鼠移植瘤模型,分析SNHG6对移植瘤生长的影响。结果SNHG6、SEPT2在BC组织和细胞中表达升高,miR-186-5p表达降低(P<0.05),选择MCF7细胞进行实验;双萤光素酶报告基因实验证实SNHG6、SEPT2与miR-186-5p存在靶向调控关系;沉默SNHG6或过表达miR-186-5p可显著抑制MCF7细胞增殖、迁移、侵袭和EMT,增加凋亡(P<0.05);抑制miR-186-5p表达或过表达SEPT2可逆转沉默SNHG6或过表达miR-186-5p对MCF7细胞增殖、迁移、侵袭和EMT的抑制作用,减少凋亡(P<0.05)。裸鼠移植瘤实验结果显示,沉默SNHG6后,移植瘤质量降低,miR-186-5p表达水平升高,SEPT2表达降低(P<0.05)。结论沉默SNHG6可通过调节miR-186-5p/SEPT2轴,抑制BC细胞增殖、迁移、侵袭和EMT,增加BC细胞凋亡。Objective To investigate the influences of lncRNA SNHG6 on epithelial mesenchymal transition(EMT)of breast cancer(BC)cells by regulating the miR-186-5p/SEPT2 axis.Methods qRT-PCR was applied to detect the expression levels of SNHG6,miR-186-5p,and SEPT2 mRNA in BC tissues and cells,and the optimal intervention cell line was screened.Double luciferase reporter gene experiment was applied to verify the targeted regulation relationship between SNHG6,SEPT2 and miR-186-5p,EdU and CCK-8 methods were applied to measure cell proliferation,flow cytometry was applied to detect cell apoptosis.Transwell cell experiment was applied to detect the numbers of cells migration and invasion.The expressions of SEPT2,E-cadherin,N-cadherin and Vimentin were detected by Western blot test.A nude mouse xenograft model was established to analyze the effect of SNHG6 on the growth of xenografts.Results SNHG6 and SEPT2 were highly expressed in BC tissues and cells,miR-186-5p lowly expressed(P<0.05),MCF7 cells were selected for the experiment.The double luciferase reporter gene experiment confirmed that SNHG6,SEPT2 and miR-186-5p had a targeted regulatory relationship.Silencing SNHG6 or overexpression of miR-186-5p could obviously inhibit MCF7 cell proliferation,migration,invasion,and EMT,and increase apoptosis(P<0.05).Inhibiting the expression of miR-186-5p or up-regulating SEPT2 could reverse the inhibitory effects of silenting SNHG6 or overexpressing miR-186-5p on MCF7 cell proliferation,migration,invasion,and EMT,and reduce apoptosis(P<0.05).The results of the nude mouse tumor bearing experiment showed that after silencing SNHG6,the quality of the transplanted tumor decreased,the expression level of miR-186-5p increased,and the expression of SEPT2 decreased(P<0.05).Conclusion SNHG6 silencing may regulate the miR-186-5p/SEPT2 axis to inhibit BC cells proliferation,migration,invasion,and EMT,and increase BC cells apoptosis.

关 键 词：乳腺癌 上皮间质转化 lncRNA SNHG6 miR-186-5p SEPT2 

分 类 号：R737.9[医药卫生—肿瘤]