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作 者:王娟[1] 李芳琼[1] 张枝倩 王伟[1] WANG Juan;LI Fang-qiong;ZHANG Zhi-qian;WANG Wei(Dept of Clinical Lab,Tongde Hospital of Zhejiang Province,Hangzhou 310012,China;College of Medical Technology,Zhejiang Chinese Medical University,Hangzhou 310053,China)
机构地区:[1]浙江省立同德医院检验科,浙江杭州310012 [2]浙江中医药大学医学技术学院,浙江杭州310053
出 处:《中国药理学通报》2020年第7期934-939,共6页Chinese Pharmacological Bulletin
基 金:国家自然科学基金资助项目(No.81774026)。
摘 要:目的从核糖体生物合成的角度探讨雷公藤甲素(triptolide,TP)抑制肺癌细胞的分子机制。方法以不同浓度的TP作用肺癌A549细胞后,利用免疫印迹检测HCA66的表达;RT-PCR检测18S RNA的表达;流式细胞术检测细胞周期和凋亡。结果TP能明显降低HCA66蛋白的表达以及18S RNA的合成。HCA66的表达被干扰后,18S RNA的合成降低;过表达HCA66能部分逆转TP对18S RNA的抑制作用,并减弱TP对肺癌细胞的凋亡诱导和周期阻滞作用。结论TP通过降低HCA66的表达来干扰核糖体18S RNA合成,进而诱导细胞凋亡和周期阻滞。Aim To explore the molecular mechanism of triptolide inhibiting lung cancer cells from the perspective of ribosome biosynthesis.Methods The protein expression of HCA66 was evaluated by Western blot,18S RNA was detected by RT-PCR,and cell cycle apoptosis was detected by flow cytometry.Results Triptolide significantly reduced the expression of HCA66 protein and inhibited the synthesis of 18S RNA.When the expression of HCA66 was disturbed,the synthesis of 18S RNA was reduced;over-expression of HCA66 could partially reverse the inhibitory effect of triptolide on 18S RNA,and weaken the apoptosis and cycle arrest induced by triptolide in lung cancer cells.Conclusions Triptolide interferes with ribosomal 18S RNA synthesis by reducing the expression of HCA66,and then further induces apoptosis and cycle arrest.
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