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作 者:杨夏楠[1] 赵丹丹 司晗 杨平娟 樊冬梅[1] Yang Xianan;Zhao Dandan;Si Han(Department of Gynecology,The First Affiliated Hospital of Henan University of Science and Technology,Luoyang,Henan,471003,China)
机构地区:[1]河南科技大学第一附属医院妇三科,河南洛阳471003
出 处:《黑龙江医学》2023年第17期2083-2087,共5页Heilongjiang Medical Journal
摘 要:目的:探讨非SMC缩合蛋白I复合物亚单位H (non-SMS condensinⅠcomplex subunit H,NCAPH)在子宫内膜癌中的表达及其对子宫内膜癌细胞增殖、迁移、侵袭和上皮间质转化(Epithal-Mesenchymal Transition,EMT)的影响。方法:将子宫内膜癌Ishikawa和KLE细胞分为si-NC组和si-NCAPH组。基于TCGA和Kaplan-Meier Plotter数据库分析NCAPH在子宫内膜癌中的表达水平、诊断价值及与患者预后的关系。CCK-8方法检测各组细胞的增殖活性变化,划痕愈合实验和Transwell实验分别检测各组细胞的迁移和侵袭能力。qRT-PCR和Western blot检测基因表达水平。结果:NCAPH在子宫内膜癌高表达,和子宫内膜癌的不良预后相关,具有临床诊断价值。沉默NCAPH后,Ishikawa和KLE细胞的增殖能力、侵袭和迁移能力明显下降。沉默NCAPH可以诱导Ishikawa和KLE细胞中E-cadherin蛋白的表达水平升高,Vimentin和N-cadherin蛋白水平降低。结论:沉默NCAPH降低子宫内膜细胞的增殖;迁移和侵袭能力,抑制子宫内膜癌的EMT,推测NCAPH有可能成为治疗子宫内膜癌的基因靶点。Objective:To investigate the expression of non-SMC condensin I complex subunit H(non-SMS condensin Ⅰ complex subunit H,NCAPH) in endometrial cancer and its effects on endometrial cancer cell proliferation,migration,invasion and epithelial-mesenchymal transition(EMT).Methods:Endometrial cancer Ishikawa and KLE cells were divided into si-NC group and si-NCAPH group.The expression level,diagnostic value and relationship with patient prognosis of NCAPH in endometrial cancer were analyzed based on TCGA and Kaplan-Meier Plotter database.The CCK-8 method was used to detect changes in the proliferative activity of each group of cells,and the scratch healing assay and Transwell assay were used to detect the migration and invasion ability of each group of cells,respectively.And qRT-PCR and Western blot were used to detect gene expression levels.Results:NCAPH was highly expressed in endometrial cancer,correlated with poor prognosis of endometrial cancer,and had clinical diagnostic value.The proliferative capacity,invasion and migration of Ishikawa and KLE cells were significantly decreased after silencing NCAPH.Silencing NCAPH induced elevated levels of E-cadherin protein expression and decreased levels of Vimentin and N-cadherin proteins in Ishikawa and KLE cells.Conclusion:Silencing NCAPH reduces the proliferation,migration and invasion ability of endometrial cells and inhibits EMT in endometrial cancer,presumably NCAPH has the potential to be a gene target for the treatment of endometrial cancer.
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