首页|lncRNA FUT8-AS1通过调控 miR-142-5p/BCL2 轴促进上皮性卵巢癌细胞增殖、侵袭和EMT

lncRNA FUT8-AS1通过调控 miR-142-5p/BCL2 轴促进上皮性卵巢癌细胞增殖、侵袭和EMT

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目的 观察FUT8-AS1基因在上皮性卵巢癌(epithelial ovarian cancer,EOC)组织和细胞株中的表达,探讨影响EOC细胞增殖、侵袭和EMT的机制.方法 采用GEPIA2和Kaplan-Meier Plotter数据库分析FUT8-AS1在EOC组织中的表达及与患者生存期的关系.收集74例EOS组织标本和60例正常组织标本,应用RT-PCR法检测FUT8-AS1、miR-142-5p、BCL2和EMT相关基因的表达;运用CCK-8和Transwell实验检测敲低FUT8-AS1基因表达对EOC细胞CAOV3增殖和侵袭的影响.利用双荧光素酶报告分析FUT8-AS1与miR-142-5p的相互作用.结果 GEPIA2和Kaplan-Meier Plotter数据库分析发现,FUT8-AS1在EOC组织中的表达显著高于正常组织(P<0.05),FUT8-AS1高表达组的总生存率显著低于FUT8-AS1低表达组(P<0.01);FUT8-AS1基因在74例EOC组织中的表达明显高于正常组织[(2.547±1.370)vs(1.330±0.831),P<0.01]),与大网膜转移、淋巴结转移、FIGO分期和总生存期均相关(P<0.01或P<0.05),敲低FUT8-AS1基因可以抑制CAOV3细胞的体外增殖、侵袭能力和EMT(P<0.01或P<0.05).双荧光素酶报告分析系统检测显示,共转染miR-142-5p mimics和野生型FUT8-AS1-WT质粒,CAOV3细胞的荧光素酶活性明显降低(P<0.05),同时转染miR-142-5p mimics可抵消CAOV3细胞中由敲低FUT8-AS1导致的BCL2基因表达下调(P<0.05).结论 FUT8-AS1基因在EOC中呈高表达且导致预后差,敲低FUT8-AS1基因可以抑制CAOV3细胞的体外增殖、侵袭能力和EMT,FUT8-AS1基因可能通过靶向miR-142-5p/BCL2分子轴促进EOC的进展.
LncRNA FUT8-AS1 promotes proliferation,invasion,and EMT of epithelial ovarian cancer cells by regulating the miR-142-5p/BCL2 axis
Purpose To investigate the expression of FUT8-AS1 gene in epithelial ovarian cancer(EOC)tissues and cell lines and its relationship with clinical pathology and progno-sis,to investigate the effect of FUT8-AS on proliferation,inva-sion and EMT of epithelial ovarian cancer cell line and its possi-ble mechanism.Methods Based on GEPIA2 and Kaplan-Meier Plotter database,the expression of FUT8-AS1 in epithelial ovarian cancer and its effect on survival of patients with ovarian cancer were analyzed,the expression levels of FUT8-AS1 miR-142-5p,BCL2,and EMT marker genes were detected by qRT-PCR,CCK-8 and Transwell assays were used to detect the effect of abnormal expression of FUT8-AS1 gene on proliferation and invasion of CAOV3 cells.The interaction between FUT8-AS1 and miR-142-5p was verified by Dual-luciferase reporter assay sys-tem.Results Using GEPIA2 and Kaplan-Meier Plotter data-bases,it was found that the expression of FUT8-AS1 in epitheli-al ovarian cancer tumor tissue was significantly higher than that in normal tissue(P<0.05),and the overall survival rate of the high expression group of FUT8-AS1 was significantly lower than that of the low expression group of FUT8-AS1(P<0.01).The expression of FUT8-AS1 gene in 74 cases of epithelial ovarian cancer tissue was significantly higher than that of normal tissue[(2.547±1.370)vs(1.330±0.831),P<0.01],and was associated with greater omentum metastasis,lymph node metas-tasis,FIGO staging,and survival(P<0.01).Knocking down the FUT8-AS1 gene can inhibit the in vitro proliferation and in-vasion ability of epithelial ovarian cancer cell line CAOV3(P<0.01 or P<0.05).The results of dual luciferase reporter gene detection showed that co transfection with miR-142-5p mimics and FUT8-AS1-WT plasmids significantly reduced the luciferase activity of CAOV3 cells(P<0.05).Transfection with miR-142-5p mimics could offset the downregulation of BCL2 gene ex-pression caused by knocking down FUT8-AS1 in CAOV3 cells(P<0.05).Conclusion The FUT8-AS1 gene is highly ex-pressed in EOC and leads to poor prognosis.Knocking down the FUT8-AS1 gene can inhibit the in vitro proliferation,invasion,and EMT of CAOV3 cells.Mechanistically,the FUT8-AS1 gene may promote the progression of EOC by targeting the miR-142-5p/BCL2 molecular axis.

ovarian neoplasmepithelial ovarian cancerFUT8-AS1miR-142-5pprognosisproliferationinvasionEMT

王娟、刘蕾蕾、郝雅丽、康山

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河北医科大学第四医院妇产科,石家庄 050011

卵巢肿瘤 上皮性卵巢癌 FUT8-AS1 miR-142-5p 预后 增殖 侵袭 EMT

河北省自然基金重点项目河北省精准医学联合基金培育项目

H2020206651H2020206385

2024

临床与实验病理学杂志
安徽医科大学,中华医学会安徽分会

临床与实验病理学杂志

CSTPCD北大核心
影响因子:0.776
ISSN:1001-7399
年,卷(期):2024.40(9)