首页|UCH-L3基因沉默对人乳腺癌细胞MCF7生物学功能的影响

UCH-L3基因沉默对人乳腺癌细胞MCF7生物学功能的影响

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目的:探讨沉默UCH-L3 基因对非三阴性乳腺癌细胞MCF7 生物学功能的影响.方法:使用靶向UCH-L3 的siRNA转染MCF7 细胞,构建UCH-L3 沉默表达模型.采用实时荧光定量PCR和Western blot分别检测UCH-L3 的mRNA和蛋白表达水平.使用CCK8 法和克隆形成实验检测细胞增殖和克隆形成能力.采用Transwell法评估细胞侵袭能力.结果:经过3 种不同siRNA的基因沉默处理,UCH-L3-001显示出最显著的沉默效果,mRNA表达水平降低至空白对照组的 24.7%,蛋白表达水平降低至空白对照组的32.0%;相比空白对照组,UCH-L3-001 siRNA沉默导致MCF7 细胞的增殖率下降 17.5%,克隆形成能力下降57.8%,迁移克隆数减少 55.0%,细胞凋亡率增加 61.6%.结论:沉默UCH-L3 能够有效抑制MCF7 细胞增殖和克隆形成能力,同时降低细胞侵袭能力并促进细胞凋亡,有望成为一种治疗非三阴性乳腺癌的新策略.
Effect of UCH-L3 Gene Silencing on the Biological Function of Human Breast Cancer Cell MCF7
Objective:To investigate the effect of silencing UCH-L3 gene on the biological function of non-triple-negative breast cancer cell strain MCF7.Methods:The UCH-L3 silencing expression model was constructed by transfecting MCF7 cells with UCH-L3 targeted siRNA.Real-time quantitative PCR and Western blot were used to detect the expression levels of mRNA and protein,respectively.Cell proliferation and clonogenesis were measured by CCK8 test and clone formation assay.The cell invasion ability was evaluated by the transwell method.Results:After silencing processing by 3 different siRNAs,UCH-L3-001 showed the most obvious silencing effect,the mRNA expression level decreased to 24.7%of the control group,and the protein expression level de-creased to 32.0%of the control group.Compared with the black control group,UCH-L3-001 siRNA silencing,decreased the pro-liferation rate of MCF7 cells by 17.5%,the cloning capacity by 57.8%,the number of migrating clones by 55.0%,and increased the apoptosis rate by 61.6%.Conclusion:Silencing UCH-L3 can effectively inhibit the proliferation and clonogenesis of MCF7 cells,and reduce the invasion ability and promote cell apoptosis,which is expected to be a new strategy for the treatment of non-tri-ple-negative breast cancer.

UCH-L3gene silencingnon triple negative breast cancerproliferationinvasion

刘振华

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长治医学院基础医学部基础医学研究所感染与免疫实验室(山西 长治 046000)

UCH-L3 基因沉默 非三阴性乳腺癌 增殖 侵袭

2024

长治医学院学报
长治医学院

长治医学院学报

影响因子:0.609
ISSN:1006-0588
年,卷(期):2024.38(6)