下调miR-4295靶向CDKN1 A调控胶质瘤U251细胞增殖和侵袭

Chinese Journal of Gerontology(2021)

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Abstract
目的 探讨下调miR-4295对胶质瘤U251细胞增殖和侵袭影响和靶向调控机制.方法 在胶质瘤U251细胞中转染miR-4295 inhibitor,qRT-PCR检测下调效果,四甲基偶氮唑蓝(MTT)比色法分析细胞增殖情况,流式细胞术检测凋亡情况,Transwell小室测定细胞侵袭和迁移能力变化.在线靶基因预测软件预测CDKN1A可能为miR-4295的靶基因,荧光素酶报告系统鉴定靶向关系.在胶质瘤U251细胞中共转染miR-4295 inhibitor、CDKN1A siRNA,同样利用上述方法分析CD-KN1A siRNA对下调miR-4295的胶质瘤细胞增殖、凋亡、侵袭和迁移能力影响.结果 anti-miR-4295组miR-4295水平显著低于control组及anti-NC组(P<0.05).anti-miR-4295组细胞OD值均显著低于control组及anti-NC组,而凋亡率显著高于con-trol组、anti-NC组(均P<0.05).anti-miR-4295组迁移和侵袭数目均显著低于control组及anti-NC组(均P<0.05).anti-miR-4295组CDKN1A蛋白水平显著高于control组及anti-NC组(均P<0.05).anti-miR-4295+si-CDKN1A组CDKN1A蛋白水平、凋亡率显著低于anti-miR-4295+si-NC组,而细胞OD值、侵袭和迁移数目均显著高于antimiR-4295+si-NC组(均P<0.05).结论 下调miR-4295靶向负调控CDKN1A抑制胶质瘤U251细胞增殖和侵袭.
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