肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2013年
5期
300-302,305
,共4页
黑色素瘤%miRNA%基因转染%细胞增殖%细胞凋亡
黑色素瘤%miRNA%基因轉染%細胞增殖%細胞凋亡
흑색소류%miRNA%기인전염%세포증식%세포조망
Melanoma%miRNA%Gene transfection%Cell proliferation%Cell apotosis
目的 进一步探讨miR-33对黑色素瘤B16F10细胞株增殖和凋亡的影响.方法 构建靶向miR-33的高表达mimics及inhibitor干扰单链,将同一株B16F10细胞分为5组:空白组、miR-33mimics组、mimics对照组、miR-33 inhibitor组、inhibitor对照组,运用脂质体转染技术将对应基因导入B16F10细胞中,从RNA水平和细胞水平分析miR-33对B16F10细胞增殖和凋亡的影响.结果 miR-33mimics组对应基因表达(1773.3±245.83)高于空白组,差异有统计学意义(P＜0.01)；miR-33 inhibitor组中对应基因相对表达(0.6973±0.1958)低于空白组和inhibitor对照组,但差异无统计学意义；miR-33mimics组与空白组相比细胞生长呈下降趋势,在转染后48 h(1.1875±0.0502)及72 h(1.7500±0.0933)趋势明显,差异均有统计学意义(均P＜ 0.05)；miR-33 mimics组细胞凋亡率[(1.8050±0.2050)％]高于空白组[(11300±0.1414)％](P＜0.05)；与空白组相比,miR-33 mimics组G1期细胞比例[(62.7000±1.7321)％]增加,S期细胞比例[(23.4000±2.5044)％]减少,差异均有统计学意义(均P＜ 0.05).结论 miR-33在高表达时抑制B16F10细胞增殖,促进细胞凋亡.
目的 進一步探討miR-33對黑色素瘤B16F10細胞株增殖和凋亡的影響.方法 構建靶嚮miR-33的高錶達mimics及inhibitor榦擾單鏈,將同一株B16F10細胞分為5組:空白組、miR-33mimics組、mimics對照組、miR-33 inhibitor組、inhibitor對照組,運用脂質體轉染技術將對應基因導入B16F10細胞中,從RNA水平和細胞水平分析miR-33對B16F10細胞增殖和凋亡的影響.結果 miR-33mimics組對應基因錶達(1773.3±245.83)高于空白組,差異有統計學意義(P＜0.01)；miR-33 inhibitor組中對應基因相對錶達(0.6973±0.1958)低于空白組和inhibitor對照組,但差異無統計學意義；miR-33mimics組與空白組相比細胞生長呈下降趨勢,在轉染後48 h(1.1875±0.0502)及72 h(1.7500±0.0933)趨勢明顯,差異均有統計學意義(均P＜ 0.05)；miR-33 mimics組細胞凋亡率[(1.8050±0.2050)％]高于空白組[(11300±0.1414)％](P＜0.05)；與空白組相比,miR-33 mimics組G1期細胞比例[(62.7000±1.7321)％]增加,S期細胞比例[(23.4000±2.5044)％]減少,差異均有統計學意義(均P＜ 0.05).結論 miR-33在高錶達時抑製B16F10細胞增殖,促進細胞凋亡.
목적 진일보탐토miR-33대흑색소류B16F10세포주증식화조망적영향.방법 구건파향miR-33적고표체mimics급inhibitor간우단련,장동일주B16F10세포분위5조:공백조、miR-33mimics조、mimics대조조、miR-33 inhibitor조、inhibitor대조조,운용지질체전염기술장대응기인도입B16F10세포중,종RNA수평화세포수평분석miR-33대B16F10세포증식화조망적영향.결과 miR-33mimics조대응기인표체(1773.3±245.83)고우공백조,차이유통계학의의(P＜0.01)；miR-33 inhibitor조중대응기인상대표체(0.6973±0.1958)저우공백조화inhibitor대조조,단차이무통계학의의；miR-33mimics조여공백조상비세포생장정하강추세,재전염후48 h(1.1875±0.0502)급72 h(1.7500±0.0933)추세명현,차이균유통계학의의(균P＜ 0.05)；miR-33 mimics조세포조망솔[(1.8050±0.2050)％]고우공백조[(11300±0.1414)％](P＜0.05)；여공백조상비,miR-33 mimics조G1기세포비례[(62.7000±1.7321)％]증가,S기세포비례[(23.4000±2.5044)％]감소,차이균유통계학의의(균P＜ 0.05).결론 miR-33재고표체시억제B16F10세포증식,촉진세포조망.
Objective To further approach the effect of miR-33 to melanoma cells line B16F10 proliferation and apoptosis.Methods Constructing targeted miR-33 over-expression mimics and inhibitor,the same B16F10 cells were divided into five groups,control group,miR-33 mimics group,mimics control group,miR-33 inhibitor group,inhibitor control group,then gene transfer technology was used to transfer corresponding gene into B16F10 cells.The effect of miR-33 on B16F10 cell' s proliferation and apoptosis were analysed.Results The relative miR-33 gene expression of miR-33 mimics group (1773.3±245.83) was higher than that of control group,which had statistical significance (P ＜ 0.01).The gene expression of miR-33 inhibitor group (0.6973±0.1958) was lower than those of control group and inhibitor control group.The cell growth rate of miR-33 mimics group was lower than those of control group and the trend after transfection 48 h (1.1875±0.0502) and 72 h (1.7500±0.0933) was significant (P ＜ 0.05).The cell apoptotic ratio of miR-33 mimics group [(1.8050±0.2050) ％] was higher than that of control group [(1.13000±0.1414) ％] (P ＜ 0.05).Compared with control group the cell proportion ofG1 period in miR-33 mimics group [(62.7000±1.7321) ％]increased,the cell proportion of S period [(23.4000±2.5044) ％] decreased,both of them had statistical significance (both P ＜ 0.05).Conclusion miR-33 over-expression can restrain the proliferation of B16F10 cells line,promote B16F10 cells' apoptosis.
