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作 者:陈希[1] 陶少宇[1] 王开阳[1] CHEN Xi;TAO Shaoyu;WANG Kaiyang(The Second Affiliated Hospital of Nanchang University,Nanchang 330000,China)
出 处:《华夏医学》2025年第2期41-47,共7页Acta Medicinae Sinica
基 金:江西省卫生健康委科技计划项目(202310487)。
摘 要:目的探讨长链非编码RNA NEAT1(IncNEAT1)通过竞争性结合miR-3619-5p调控丝点蛋白M(CENPM)表达在肝癌细胞侵袭转移中的作用。方法选取100例临床肝癌患者外科手术切除的组织标本,采用蛋白质印迹法(Western blot)、实时荧光定量聚合酶链反应(RT-qPCR)观察LncNEAT1、CENPM和miR-3619-5p的表达情况,采用划痕实验观察肝癌细胞侵袭转移的影响,并探讨在临床肝癌组织标本中LncNEAT1与CENPM表达的相关性。结果在临床肝癌及癌旁正常组织中,LncNEAT1与CENPM在肝癌组织中均呈高表达,差异有统计学意义(P<0.05),LncNEAT1与CENPM表达呈正相关(r=0.450,P<0.05)。在肝癌细胞中上调LncNETA1表达,CENPM表达增加(P<0.05),肝癌细胞的侵袭迁移能力增加(均P<0.05)。在肝癌细胞中上调LncNEAT1表达,miR-3619-5p表达明显下降(P<0.05);上调LncNEAT1表达同时抑制miR-3619-5p表达,CENPM表达未发生明显变化(P>0.05)。结论LncNETA1通过竞争性结合miR-3619-5p促进CENPM的表达,从而促进肝癌细胞的侵袭转移,并为肝癌的治疗提供新的策略和潜在的治疗靶点。Objective To investigate the role of long noncoding RNA NEAT1(IncNEAT1)in the regulation of kinetochore protein M(CENPM)expression in the invasion and metastasis of hepatocellular carcinoma(HCC)cells by competitive binding to miR-3619-5p.Methods The tissues of 100 clinical HCC patients were selected,and the expression of LncNEAT1,CENPCR and miR-3619-5p was Western blotting and real-time quantitative polymerase chain reaction(qRT-PCR),scratch assay was used to observe the effect of HCC cell invasion and metastasis,and to explore the correlation between LncNEAT1 and CENPM expression in clinical HCC tissue specimens.Results In clinical HCC and adjacent normal tissues,LncNEAT1 and CENPM were highly expressed in HCC tissues,showing a statistically significant difference(P<0.05),and LncNEAT1 was positively correlated with CENPM expression(r=0.450,P<0.05).Up-regulation of LncNETA1 expression in HCC cells,increased CENPM expression(all P<0.05),and increased invasion and migration capacity of HCC cells(all P<0.05).Up-regulated LncNEAT1 expression in HCC cells,miR-3619-5p expression decreased significantly(P<0.05).Increased LncNEAT1 expression also suppressed miR-3619-5p expression,and CENPM expression did not change significantly(P>0.05).Conclusion LncNETA1 promotes the expression of CENPM by competitively binding to miR-3619-5p,thus promoting the invasion and metastasis of HCC cells and providing new strategies and potential therapeutic targets for the treatment of HCC.
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