FAM83H-AS1促进子宫内膜癌细胞系Ishikawa上皮-间质转化和血管生成

doi:10.16352/j.issn.1001-6325.2026.04.0517

摘要/Abstract

摘要： 目的探究FAM83H-AS1对子宫内膜癌细胞上皮间质转化及血管生成的作用及机制。方法人子宫内膜癌细胞Ishikawa培养后,分为空白组、FAM83H-AS siRNA组(转染FAM83H-AS siRNA)、miR-4684-5p mimics组(转染miR-4684-5p mimics)、FAM83H-AS siRNA＋miR-4684-5p mimics组(共转染FAM83H-AS siRNA与miR-4684-5p mimics)。Transwell小室法检测细胞的侵袭;Matrigel基质胶法检测细胞管腔形成;Western blot检测上皮间质转化标志蛋白E-cadherin和vimentin,双荧光素酶报告实验检测FAM83H-AS1与miR-4684-5p靶向关系;qPCR检测FAM83H-AS1及miR-4684-5p表达。结果与空白组比较,FAM83H-AS siRNA组及miR-4684-5p mimics组Ishikawa细胞中FAM83H-AS1降低、miR-4684-5p升高(P＜0.05);与FAM83H-AS siRNA组及miR-4684-5p mimics组比较,FAM83H-AS siRNA＋miR-4684-5p mimics组Ishikawa细胞中FAM83H-AS1降低、miR-4684-5p升高(P＜0.05),其中FAM83H-AS siRNA组与miR-4684-5p mimics组的差异无统计学意义。与空白组比较,FAM83H-AS siRNA组及miR-4684-5p mimics组细胞侵袭数量、管腔形成数量及蛋白vimentin均降低,E-cadherin升高(P＜0.05);与FAM83H-AS siRNA组及miR-4684-5p mimics组比较,FAM83H-AS siRNA＋miR-4684-5p mimics组细胞侵袭数量、管腔形成数量及蛋白vimentin均降低,E-cadherin升高(P＜0.05),其中FAM83H-AS siRNA组与miR-4684-5p mimics组的差异无统计学意义。双荧光素酶报告实验结果显示,转染miR-4684-5p mimics,FAM83H-AS1 3′UTR-WT组活性显著降低(P＜0.05),但FAM83H-AS1 3′UTR-MUT组的影响并不显著。结论在子宫内膜癌细胞系Ishikawa中,敲低FAM83H-AS1及上调miR-4684-5p,抑制上皮-间质转化和血管生成,可能通过靶向调节miR-4684-5p发挥作用。

关键词: 子宫内膜癌, FAM83H-AS1, miR-4684-5p, 上皮-间质转化, 血管生成

Abstract: Objective To investigate the effect and mechanism of FAM83H-AS1 on epithelial-mesenchymal transition (EMT) and angiogenesis in endometrial cancer cells. Methods Human endometrial cancer Ishikawa cells were divided into four groups: Blank group, FAM83H-AS1 siRNA group (transfected with FAM83H-AS1 siRNA), miR-4684-5p mimics group (transfected with miR-4684-5p mimics), and FAM83H-AS1 siRNA + miR-4684-5p mimics group (co-transfected with FAM83H-AS1 siRNA and miR-4684-5p mimics). Cell invasion was detected by Transwell assay; tube formation was detected by Matrigel assay; the EMT marker proteins E-cadherin and Vimentin were detected by Western blot; the targeted relationship between FAM83H-AS1 and miR-4684-5p was detected by dual-luciferase reporter assay; and the expression levels of FAM83H-AS1 and miR-4684-5p were detected by qPCR. Results Compared with the Blank group, the expression of FAM83H-AS1 was decreased and the expression of miR-4684-5p was increased in FAM83H-AS1 siRNA group and the miR-4684-5p mimics group(P＜0.05). Compared with the FAM83H-AS1 siRNA group or the miR-4684-5p mimics group, the expression of FAM83H-AS1 was decreased and the expression of miR-4684-5p was increased in the FAM83H-AS1 siRNA + miR-4684-5p mimics group (P＜0.05), among which there was no statistically significant difference between the FAM83H-AS1 siRNA group and the miR-4684-5p mimics group. Compared with the blank group, the number of cell invasions, tube formations, and the protein level of Vimentin were all decreased, while E-cadherin was increased in the FAM83H-AS1 siRNA group and the miR-4684-5p mimics group (P＜0.05). Compared with the FAM83H-AS1 siRNA group or the miR-4684-5p mimics group, the number of cell invasions, tube formations, and the protein level of vimentin were all decreased, while E-cadherin was increased in the FAM83H-AS1 siRNA+miR-4684-5p mimics group (P＜0.05), among which there was no statistically significant difference between the FAM83H-AS1 siRNA group and the miR-4684-5p mimics group. The dual-luciferase reporter assay showed that after transfection with miR-4684-5p mimics, the activity in the FAM83H-AS1 3′UTR-WT group was significantly reduced (P＜0.05), whereas the effect on the FAM83H-AS1-3′UTR-MUT group was not significant. Conclusions In the endometrial cancer cell line Ishikawa, knockdown of FAM83H-AS1 or overexpression of miR-4684-5p inhibits epithelial-mesenchymal transition and angiogenesis, an effect mediated by the targeted regulation of miR-4684-5p.

Key words: FAM83H-AS1, miR-4684-5p, endometrial cancer, epithelial-mesenchymal transition (EMT), angiogenesis

中图分类号:

R737.33

严鲁豫, 王超, 封硕. FAM83H-AS1促进子宫内膜癌细胞系Ishikawa上皮-间质转化和血管生成[J]. 基础医学与临床, 2026, 46(4): 517-523.

YAN Luyu, WANG Chao, FENG Shuo. FAM83H-AS1 promotes epithelial-mesenchymal transition and angiogenesis in the endometrial cancer cell line Ishikawa[J]. Basic & Clinical Medicine, 2026, 46(4): 517-523.

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