MALAT-1沉默对膀胱癌细胞增殖、凋亡及caspase-3表达的影响

Effect of MALAT-1 Silencing on Proliferation,Apoptosis and Expression of Caspase-3 in Bladder Cancer Cells

目的检测MALAT-1在正常膀胱组织和膀胱癌组织间的表达差异,探讨MALAT-1沉默对膀胱癌细胞增殖、凋亡及caspase-3表达的影响。方法 RT-PCR检测膀胱癌组织及正常膀胱组织中MALAT-1基因的表达; CCK-8比色实验检测MALAT-1沉默和MALAT-1正常表达的膀胱癌EJ细胞的增殖; TUNEL免疫荧光法检测MALAT-1沉默和MALAT-1正常表达膀胱癌EJ细胞的凋亡; Western blot法检测MALAT-1沉默和MALAT-1正常表达的膀胱癌EJ细胞中caspase-3蛋白的表达。结果膀胱癌组织中MALAT-1的表达显著高于正常膀胱上皮组织; MALAT-1沉默细胞的增殖能力显著弱于MALAT-1正常表达的细胞; MALAT-1沉默细胞的凋亡显著高于MALAT-1正常表达的细胞; MALAT-1沉默细胞caspase-3蛋白的表达显著高于MALAT-1正常表达的细胞。结论 MALAT-1在膀胱癌组织中的表达被激活,MALAT-1能促进膀胱癌细胞的增殖,抑制膀胱癌细胞的凋亡,这种抑制作用可能是通过直接调控caspase-3的表达而实现的。

Objective To detect the expression of MALAT-1 in normal bladder tissue and bladder cancer tissues and to investigate the effect of MALAT-1 silencing on the proliferation,apoptosis and the expression of caspase-3 in bladder cancer cells.Methods MALAT-1 gene expression in bladder cancer tissues and normal bladder epithelial tissues was detected by RT-PCR.CCK-8 colorimetric assay was used to detect the proliferation of bladder cancer EJ cells with MALAT-1 silencing and normal expression of MALAT-1.TUNEL Immunofluorescence was used to detect the apoptosis of MALAT-1 Silencing and MALAT-1 Normal Expression in bladder cancer EJ cells.Western blot detection was used to detect the caspase-3 protein expression on MALAT-1 silence and MALAT-1 normal expression of bladder cancer EJ cells.Results The expression of MALAT-1 in bladder cancer was significantly higher than that in normal bladder epithelial tissue.The proliferation of MALAT-1 silenced cells was significantly weaker than that of MALAT-1 normally expressed.MALAT-1 silencing cells were significantly more apoptotic than MALAT-1 normally expressing cells.The expression of caspase-3 in MALAT-1 silenced cells was significantly higher than that in MALAT-1 normal expression.Conclusion The expression of MALAT-1 in bladder cancer is abnormally activated.MALAT-1 can promote the proliferation of bladder cancer cells,Inhibit the apoptosis of bladder cancer cells,this inhibition may be through the direct regulation of caspase-3 expression.