摘要
目的探讨lncRNA HNF1A⁃AS1在口腔癌中的作用及机制。方法测定HNF1A⁃AS1、miR⁃320d及PBX3在HSC⁃6和HOK细胞中的表达。HNF1A⁃AS1、miR⁃320d、PBX3表达被上调或沉默,HSC⁃6细胞增殖、侵袭和上皮间质转化(EMT)能力分别通过MTT、Transwell和Western blot测定。双荧光素酶报告基因实验分析HNF1A⁃AS1、miR⁃320d、PBX3之间的关系。结果与HOK细胞相比,HSC⁃6细胞中HNF1A⁃AS1表达量升高,差异有统计学意义(P<0.01)。下调HNF1A⁃AS1表达抑制了HSC⁃6细胞增殖、侵袭和EMT。HNF1A⁃AS1靶向miR⁃320d。与HOK细胞相比,HSC⁃6细胞中miR⁃320d表达量降低,差异有统计学意义(P<0.01)。下调miR⁃320d表达促进了HSC⁃6细胞增殖、侵袭和EMT。上调HNF1A⁃AS1表达通过miR⁃320d促进了HSC⁃6细胞增殖、侵袭和EMT。miR⁃320d靶向PBX3。与HOK细胞相比,HSC⁃6细胞中PBX3表达量上升,差异有统计学意义(P<0.01)。下调PBX3表达抑制了HSC⁃6细胞增殖、侵袭和EMT。下调HNF1A⁃AS1表达通过miR⁃320d抑制了PBX3表达。结论LncRNA HNF1A⁃AS1通过miR⁃320d促进PBX3的表达,从而促进口腔癌的发展。
Objective To explore the role and mechanism of lncRNA HNF1A⁃AS1 in oral cancer.Methods The expression levels of HNF1A⁃AS1,miR⁃320d and PBX3 in HSC⁃6 and HOK cells were determined.The expression of HNF1A⁃AS1,miR⁃320d and PBX3 were up⁃regulated or silenced,and the proliferation,invasion and EMT ability of HSC⁃6 cells were determined by MTT,Transwell and Western blot,respectively.The relationship between HNF1A⁃AS1,miR⁃320d and PBX3 was analyzed by double luciferase reporter gene assay.Results Compared with HOK cells,the expression of HNF1A⁃AS1 in HSC⁃6 cells was significantly increased(P<0.01).Down⁃regulation of HNF1A⁃AS1 expression inhibited proliferation,invasion and EMT of HSC⁃6 cells.HNF1A⁃AS1 targeted miR⁃320d.Compared with HOK cells,the expression of miR⁃320d in HSC⁃6 cells was decreased,and the difference was statistically significant(P<0.01).Down⁃regulation of miR⁃320d expression promoted proliferation,invasion and EMT of HSC⁃6 cells.Up⁃regulation of HNF1A⁃AS1 expression promoted the proliferation,invasion and EMT of HSC⁃6 cells through miR⁃320d.miR⁃320d targeted PBX3.Compared with HOK cells,the expression of PBX3 in HSC⁃6 cells was increased,and the difference was statistically significant(P<0.01).Down⁃regulation of PBX3 expression inhibited the proliferation,invasion and EMT of HSC⁃6 cells.Down⁃regulation of HNF1A⁃AS1 expression inhibited PBX3 expression through miR⁃320d.Conclusion LncRNA HNF1A⁃AS1 facilitates PBX3 expression by targeting miR⁃320d to promote oral cancer development.
作者
司亚静
张建丽
郑雪莉
SI Yajing;ZHANG Jianli;ZHENG Xueli(Department of Stomatology,The First Affiliated Hospital of Henan University of Science and Technology,Luoyang,Henan Province,China,471003)
出处
《分子诊断与治疗杂志》
2022年第12期2044-2049,2054,共7页
Journal of Molecular Diagnostics and Therapy
基金
河南省高等学校重点科研项目(18B416002)。
