RP11-386G11.10在三阴性乳腺癌组织中的表达及其对细胞增殖和迁移的影响  

Expression of RP11-386G11.10 in triple-negative breast cancer tissues and its effect on cell proliferation and migration

作　　者：张建良 贾光伟 熊辉[1] 朱婷[2] 苏阳 Zhang Jianliang;Jia Guangwei;Xiong Hui;Zhu Ting;Su Yang(Department of Thyroid and Breast Surgery,Nanyang First People’s Hospital Affiliated to Henan University,Nanyang 473010;Department of Oncology,The First Affiliated Hospital of Guangzhou Medical University,Guangzhou 510120,China)

机构地区：[1]河南大学附属南阳市第一人民医院甲状腺乳腺外科,南阳473010 [2]广州医科大学附属第一医院肿瘤科,广州510120

出　　处：《解剖学杂志》2024年第3期211-216,257,共7页Chinese Journal of Anatomy

基　　金：国家自然科学基金(81902991);南阳市科技局课题(JCQY001)。

摘　　要：目的:探讨三阴性乳腺癌组织中长链非编码RNA(lncRNA)RP11-386G11.10的表达及其通过调控miR-1299-3p/葡萄糖转运蛋白-1(GLUT-1)分子轴对三阴性乳腺癌细胞增殖和迁移的影响。方法:收集46例三阴性乳腺癌组织及癌旁组织,RT-qPCR检测RP11-386G11.10在其中的表达以及在正常乳腺上皮MCF-10A细胞和三阴性乳腺癌细胞系(MDA-MB-435、CAL-51、BT-549、MDA-MB-231)中的表达。si-NC慢病毒和si-RP11-386G11.10慢病毒感染BT-549细胞(即si-NC组和si-RP11-386G11.10组),克隆形成实验和细胞划痕实验分别检测细胞增殖和迁移能力;RT-qPCR检测感染后BT-549细胞中miR-1299-3p和GLUT-1 mRNA的表达;双荧光素酶报告基因实验验证RP11-386G11.10与miR-1299-3p的靶向关系。RT-qPCR检测GLUT-1 mRNA在三阴性乳腺癌组织中的表达;Pearson法检测RP11-386G11.10与GLUT-1 mRNA在三阴性乳腺癌组织中表达的关系。免疫印迹检测沉默RP11-386G11.10对BT-549细胞中GLUT-1蛋白以及JAK2/STAT3通路蛋白表达的影响。结果:与癌旁组织相比,三阴性乳腺癌组织中RP11-386G11.10的表达显著升高。与MCF-10A细胞相比,三阴性乳腺癌细胞系(MDA-MB-435、CAL-51、BT-549、MDA-MB-231)中RP11-386G11.10的表达均显著升高。与si-NC组BT-549细胞相比,si-RP11-386G11.10组细胞增殖能力和迁移能力均显著降低,miR-1299-3p表达显著升高,GLUT-1mRNA表达显著降低。RP11-386G11.10能够靶向互补结合miR-1299-3p。与癌旁组织相比,三阴性乳腺癌组织中GLUT-1 mRNA表达显著增加;Pearson法分析显示RP11-386G11.10与GLUT-1 mRNA在三阴性乳腺癌组织中的表达呈正相关。与si-NC组BT-549细胞比较,si-RP11-386G11.10组细胞中GLUT-1蛋白表达显著降低,JAK2/STAT3通路转导被抑制。结论:RP11-386G11.10在三阴性乳腺癌中表达显著上调,沉默RP11-386G11.10能够抑制三阴性乳腺癌BT-549细胞的增殖能力和迁移能力,其作用机制可能与靶向调控miR-1299-3p/GLUT-1分子轴有关。Objective:To explore the expression of lnc RNA RP11-386G11.10 in triple-negative breast cancer tissue and its effect on the proliferation and migration of triple-negative breast cancer cells through regulating the mi R-1299-3p/GLUT-1 molecular axis.Methods:A total of 46 cases of triple-negative breast cancer tissue and adjacent tissue were collected,and RT-q PCR was used to detect the presence of RP11-386G11.10 in triple-negative breast cancer tissue,the expression of RP11-386G11.10 in normal breast epithelial MCF-10A cells and that in triplenegative breast cancer cell lines(MDA-MB-435,CAL-51,BT-549,MDA-MB-231).BT-549 cells were infected with si-NC lentivirus and si-RP11-386G11.10 lentivirus,and they were named si-NC group and siRP11-386G11.10 group respectively.The proliferation and migration abilities of BT-549 cells were detected through colony formation assay and cell scratch assay,respectively.RT-q PCR was used to detect the expression of mi R-1299-3p and GLUT-1 m RNA in BT-549 cells after infection.A dual-luciferase reporter gene experiment was used to verify the targeting relationship between RP11-386G11.10 and mi R-1299-3p.RT-q PCR was used to detect the expression of GLUT-1 m RNA in triple-negative breast cancer tissues.The Pearson method was used to detect the relationship between the expression of RP11-386G11.10 and GLUT-1 m RNA in triple-negative breast cancer tissues.Western blotting was used to detect the effect of silencing RP11-386G11.10 on the expression of GLUT-1 protein and JAK2/STAT3 pathway proteins in BT-549 cells.Results:Compared with adjacent tissues,the expression of RP11-386G11.10 in triple-negative breast cancer tissues was significantly increased.Compared with MCF-10A cells,the expression levels of RP11-386G11.10 in triple-negative breast cancer cell lines(MDA-MB-435,CAL-51,BT-549,MDA-MB-231) were all significantly increased.Compared with BT-549 cells in the si-NC group,the proliferation and migration abilities of cells in siRP11-386G11.10 group were significantly reduced.Compared with

关 键 词：三阴性乳腺癌 长链非编码RNA RP11-386G11.10 微小RNA 葡萄糖转运蛋白-1 

分 类 号：R365[医药卫生—病理学]