微小RNA-454-3p通过靶向BUB1促进人结直肠癌细胞增殖和诱导凋亡  被引量:1

MicroRNA-454-3p promotes the proliferation of human colorectal cancer cells and induces apoptosis by targeting BUB1

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作  者:杨振[1] 蒲鸣龙 董新华[1] 杨鸿炜 朱阿丽 Yang Zhen;Pu Minglong;Dong Xinhua;Yang Hongwei;Zhu Ali(Department of Gastrointestinal Surgery,the First Affiliated Hospital of Zhengzhou University 450052,China;不详)

机构地区:[1]郑州大学第一附属医院胃肠外科,450052 [2]不详

出  处:《中华实验外科杂志》2021年第8期1507-1510,共4页Chinese Journal of Experimental Surgery

基  金:河南省教育厅高等学校重点科研项目(14B320014)。

摘  要:目的探讨微小RNA(miR)-454-3p在结直肠癌细胞增殖和侵袭中的作用及其可能分子学机制。方法选取2019年6月1日至2019年8月31日于郑州大学第一附属医院原发性结直肠癌的患者19例肿瘤组织及其对应的癌旁组织标本。应用应用荧光定量聚合酶链反应(RT-qPCR)技术检测样本中miR-454-3p的表达水平。通过细胞计数试剂盒(CCK-8)和Transwell实验评估结直肠癌细胞系CW-2、SW620细胞增殖和迁移侵袭能力。双荧光素酶报告基因验证miR-454-3p对下游靶基因BUB1蛋白的调控作用。组间采用配对样本t检验。结果与邻近正常组织比较,肿瘤组织中miR-454-3p表达上调(P<0.01),通过CCK-8测定miR-454-3p-inhibitor细胞的增殖,发现其显著低于miR-454-3p-NC组细胞(P<0.05)。transwell实验表明,与对照细胞比较,转染miR-454-3p-inhibitor的CW-2、SW620细胞迁移更慢,侵袭性更小。双荧光素酶报告分析。结果显示,miR-454-3p模拟和BUB1-wt共转染组的荧光素酶活性相对低于BUB1-wt和NC共转染组,而BUB1-mut组没有观察到显著变化(P<0.01)。此外,RIP分析表明,与RIPIgG比较,转染miR-454-3p模拟物导致RIP-BUB1中BUB1的显著上调(P<0.01)。qRT-PCR实验表明结直肠组织中BUB1和miR-454-3p表达呈正相关(P<0.01)。结论miR-454-3p可通过靶向抑制BUB1基因的表达促进结直肠癌细胞的增殖和侵袭。Objective To explore the role of microRNA(miR)-454-3p in the proliferation and invasion of colorectal cancer cells and its possible molecular mechanism.Methods To explore the role of miR-454-3p in the proliferation and invasion of colorectal cancer cells and its possible molecular mechanism.Methods A total of 19 tumor tissues and their corresponding paracancerous tissue specimens from patients with primary colorectal cancer in the First Affiliated Hospital of Zhengzhou University from June 1,2019 to August 31,2019 were selected.Quantitative real time polymerase chain reaction(qRT-PCR)technology was used to detect the expression level of miR-454-3p in the samples.Cell counting kit-8(CCK-8)and migration&invasion experiments were used to evaluate the cell proliferation,migration and invasion ability of colorectal cancer cell lines CW-2 and SW620.The dual luciferase reporter gene verified the regulatory effect of miR-454-3p on the downstream target gene BUB1(budding uninhibited by benzimidazoles 1)protein.A paired sample t test was used between groups.Results Compared with nearby tissues,the expression of miR-454-3p in the tissues was up-regulated(P<0.01),through the discovery of CCK-8 supplementing miR-454-3p-inhibitor cells,it was found that it was significantly normal miR-454-3p-NC cells(P<0.05).The transwell experiment proved that,compared with control cells,CW-2 and SW620 cells transfected with miR-454-3p-inhibitor migrated more slowly and had less productivity.The bimolecular enzyme analysis report showed that miR-454-3p simulation and BUB1-wt co-transfection group′s magic mirror magic change compared to broadcast BUB1-wt and NC co-transfection group,while the BUB1-mut group was not observed significantly(P<0.01).In addition,RIP analysis evidence Compared with RIPIgG,transfection with miR-454-3p mimics resulted in a significant up-regulation of BUB1 in RIP-BUB1(P<0.01).The qRT-PCR experiment verified that the expression of BUB1 and miR-454-3p in straight tissues was positively correlated(P<0.01).Conclusion Mi

关 键 词:微小RNA 结直肠癌 增殖 侵袭 

分 类 号:R735.34[医药卫生—肿瘤]

 

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