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| 长链非编码RNA ATB调控miR-144对胶质瘤迁移和侵袭的影响 |
| Long chain non-coding RNA-ATB regulates effect of miR-144 on migration and invasion of gliomas |
| 投稿时间：2018-03-18 |
| DOI：10.3969/j.issn.1000-0399.2018.10.006 |
| 中文关键词: 胶质瘤 增殖 侵袭 凋亡 微小RNA-144 长链非编码RNA ATB |
| 英文关键词: Glioma Proliferation Invasion Apoptosis miR-144 lncRNA ATB |
| 基金项目: |
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| 中文摘要: |
| 目的 探讨长链非编码RNA ATB （lncRNA ATB）调控miR-144对胶质瘤迁移和侵袭的影响。方法 采用qPCR检测lncRNA ATB在胶质瘤组织和癌旁正常组织中的表达差异以及慢病毒si-ATB对胶质瘤细胞的转染效率情况；通过双荧光素酶报告基因进行检测lncRNA ATB和miR-144之间的关系；通过平板克隆实验检测lncRNA ATB对胶质瘤细胞株U87和U251增殖能力的影响；流式细胞术检测lncRNA ATB对胶质瘤细胞株凋亡行为的影响；Transwell实验检测lncRNA ATB对细胞株侵袭能力的影响；裸鼠体内实验检测lncRNA ATB对裸鼠移植瘤的体积和质量的影响情况。结果 胶质瘤lncRNA ATB的表达水平高于癌旁正常组织（P<0.05），高水平lncRNA ATB患者的生存率低于低水平lncRNA ATB患者；使用si-ATB1和si-ATB2分别转染胶质瘤U87和U251细胞后，lncRNA ATB的表达水平降低；过表达miR-144后，野生型lncRNA ATB的荧光素酶活性受到抑制，对突变型lncRNA ATB的荧光素酶活性影响不明显。转染si-ATB 24、48和72小时后，U87[（186.4±12.4）个比（73.6±8.6）个比（62.6±5.6）个，P<0.05]和U251细胞[（192.2±15.3）个比（63.6±6.3）个比（68.3±7.6）个，P<0.05]和U251细胞的增殖能力低于对照组；lncRNA ATB的下调提高了U87和U251凋亡百分比（P<0.05）；抑制lncRNA ATB后，U87细胞和U251细胞的细胞侵袭能力降低；与对照组相比，si-ATB组肿瘤体积和肿瘤重量均小于或低于对照组（P<0.05）。结论 lncRNA ATB通过调控miR-144的表达促进胶质瘤细胞的生物学行为。 |
| 英文摘要: |
| Objective To investigate the effects of long-chain non-coding RNA-ATB on the migration and invasion of gliomas by miR-144. Methods The expression of lncRNA ATB in glioma tissues and adjacent normal tissues and transfection efficiency of lentiviral si-ATB on glioma cells were detected by qPCR. The relationship between lncRNA ATB and miR-144 was detected by the dual luciferase reporter gene. The effect of lncRNA ATB on proliferation of glioma cell lines U87 and U251 was examined by plate cloning assay. The effect of lncRNA ATB on apoptosis of glioma cell lines was detected by flow cytometry. The effect of lncRNA ATB on the invasive ability of the cell line was assessed by Transwell assay. The effect of lncRNA ATB on the volume and quality of xenograft tumor was tested in nude mice. Results The expression of lncRNA ATB in gliomas was significantly higher than that in adjacent normal tissues[(10.21±1.32) vs (3.26±0.86), P<0.05]. The survival rate of high-level lncRNA ATB patients was lower than that of low-level lncRNA ATB patients. After transfection of glioma U87 and U251 cells with siATB1 and siATB2, the expression level of lncRNA ATB was significantly reduced. After overexpression of miR-144, the luciferase activity of wild-type lncRNA ATB was significantly inhibited, and the fluorescence of mutant lncRNA ATB was significantly reduced. The enzyme activity showed no obvious effect. After 24, 48 and 72 hours of transfection with si-ATB, the proliferation of U87 and U251 cells was significantly lower than that of their respective control groups; the down-regulation of lncRNA ATB significantly increased U87 and U251 percentage of apoptosis. After inhibiting lncRNA ATB, U87 [(14.2±0.5)% vs (7.2±0.4)% vs (4.6 ±0.4)%, P<0.05] and U251[(13.9 ±0.7)% vs (10.1 ±0.3)% vs (5.6 ±0.4)%,P<0.05] percentage of apoptosis. After inhibiting lncRNA ATB, U87 cells[(186.4±12.4) vs (73.6±8.6) vs (62.6±5.6),P<0.05] and U251 cells[(192.2±15.3) vs (63.6±6.3) vs (68.3±7.6),P<0.05] significantly decreased invasive ability; the mean tumor volume and mean tumor weight of si-ATB group was significantly lower than those of control group (P<0.05). Conclusion lncRNA ATB promotes the malignant biological behavior of glioma cells by regulating miR-144 expression. |
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