长链非编码RNA LINC01419调控结直肠癌细胞增殖、凋亡、迁移侵袭的机制  

The mechanism by which the long noncoding RNA LINC01419 regulates colorectal cancer cell proliferation,apoptosis and migration and invasion

作　　者：陈素华[1] 马天江[1] 张智慧[1] 张磊[1] 史磊[1] CHEN Suhua;MA Tianjiang;ZHANG Zhihui;ZHANG Lei;SHI Lei(Department of Oncology,Luohe Central Hospital,Luohe,Henan 462000,China)

机构地区：[1]漯河市中心医院肿瘤科,河南漯河462000

出　　处：《安徽医药》2022年第3期572-577,F0003,共7页Anhui Medical and Pharmaceutical Journal

摘　　要：目的研究长链非编码RNA(lncRNA)LINC01419调控结直肠癌细胞增殖、凋亡、迁移侵袭的机制。方法收集漯河市中心医院2015年10月至2018年5月因结直肠癌手术切除的组织标本20例,以距离结直肠癌边缘≥3 cm的癌旁正常组织标本20例为对照。实时荧光定量逆转录聚合酶链反应(qRT-PCR)检测结直肠癌组织中lncRNALINC01419和微小RNA-132-3p(miR-132-3p)表达。构建干扰lncRNALINC01419或miR-132-3p过表达的结直肠癌SW620细胞,MTT法和流式细胞术分别检测细胞增殖与凋亡,Transwell检测细胞迁移、侵袭,蛋白质印迹法(Westernblotting)检测细胞周期蛋白D1(cyclinD1)、细胞周期蛋白依赖性激酶抑制剂1A(P21)、B细胞淋巴瘤-2(Bcl-2)蛋白、Bcl-2相关X(Bax)蛋白、基质金属蛋白酶-2(MMP-2)、基质金属蛋白酶-9(MMP-9)蛋白表达。生物信息学预测结合双荧光素酶报告实验分析lncRNALINC01419和miR-132-3p的靶向关系。si-LINC01419和anti-miR-123-3p共转染,观察抑制miR-132-3p表达对干扰lncRNALINC01419诱导的SW620细胞增殖、凋亡、迁移、侵袭的影响。结果与癌旁组织[(1.00±0.09)、(1.01±0.08)]比较,结直肠癌组织中lncRNALINC01419表达量(2.74±0.26)明显增加(P<0.05),miR-132-3p表达量(0.51±0.05)显著减少(P<0.05)。干扰lncRNALINC01419或miR-132-3p过表达显著抑制SW620细胞增殖、迁移、侵袭、cyclinD1、Bcl-2、MMP-2、MMP-9蛋白表达,并促进细胞凋亡、P21、Bax蛋白表达。lncRNA LINC01419靶向调控miR-132-3p的表达。抑制miR-132-3p表达逆转了干扰lncRNALINC01419对结直肠癌细胞SW620增殖、迁移、侵袭的抑制作用,以及对细胞凋亡的促进作用。结论lncRNALINC01419通过靶向miR-132-3p调控结直肠癌细胞增殖、凋亡、迁移侵袭。Objective To study the mechanism by which the long noncoding RNA(lncRNA)LINC01419 regulates colorectal cancer cell proliferation,apoptosis,migration and invasion.Methods Twenty tissue samples from Luohe Central Hospital from October 2015 to May 2018 due to surgical resection of colorectal cancer were collected,and 20 normal tissue samples with a distance of≥3 cm from the edge of colorectal cancer were used as controls.qRT-PCR was used to detect the expression of lncRNA LINC01419 and microRNA-132-3p(miR-132-3p)in colorectal cancer tissues.After construction of lncRNA LINC01419-silenced or miR-132-3p-overexpressing colorectal cancer SW620 cells,MTT assay and flow cytometry were applied to detect cell proliferation and apoptosis,Transwell assays were employed to detect cell migration and invasion,and Western blotting was used to analyze cyclin D1,cyclin-dependent kinase in⁃hibitor 1A(P21),B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),matrix metalloproteinase-2(MMP-2),and MMP-9 pro⁃tein expression.Bioinformatics prediction combined with a dual luciferase reporter assay was used to analyze the targeting relationship between lncRNA LINC01419 and miR-132-3p.Si-LINC01419 and anti-miR-123-3p were cotransfected to observe the effect of inhibit⁃ing miR-132-3p on the proliferation,apoptosis,migration and invasion of SW620 cells induced by lncRNA LINC01419 silencing.Re⁃sults Compared with the adjacent tissues[(1.00±0.09),(1.01±0.08)],the expression of lncRNA LINC01419(2.74±0.26)in colorectal cancer tissues was significantly increased(P<0.05),while the expression of miR-132-3p(0.51±0.05)was obviously decreased(P<0.05).Silencing lncRNA LINC01419 or overexpressing miR-132-3p markedly inhibited SW620 cell proliferation,migration and invasion and cyclin D1,Bcl-2,MMP-2,and MMP-9 protein expression and promoted apoptosis and P21 and Bax protein expression.The lncRNA LINC01419 targets miR-132-3p.Inhibition of miR-132-3p reversed the inhibitory effects of interfering with lncRNA LINC01419 on the proliferation,

关 键 词：结直肠肿瘤 长链非编码RNA LINC01419 微小RNA-132-3p 增殖 凋亡 

分 类 号：R735.34[医药卫生—肿瘤]