期刊文献+

HDAC抑制剂SAHA抑制人乳腺癌细胞MCF-7的迁移和增殖 被引量:1

Inhibiting the Proliferation and Migration of Human Breast Cancer Cell MCF-7 with HDAC Inhibitor SAHA
下载PDF
导出
摘要 用组蛋白去乙酰化酶(histone deacetylase complex,HDAC)抑制剂SAHA对人乳腺癌细胞MCF-7进行处理,抑制组蛋白的去乙酰化,进而检测SAHA对MCF-7的影响.体外划痕实验与Transwell实验表明SAHA可以抑制MCF-7细胞的迁移;免疫印迹(Western blot)实验表明SAHA可以抑制迁移相关基因MYL9蛋白水平的表达.MTT实验和克隆形成实验表明SAHA可以抑制MCF-7细胞的增殖;Western blot实验与逆转录实时荧光定量PCR(RT-qPCR)实验表明SAHA能够抑制细胞周期蛋白标志基因CyclinD1、CDK4的表达,促进周期蛋白激酶抑制剂p21的表达. Histone deacetylase complex(HDAC)inhibitor SAHA was used to deal with human breast cancer cell MCF-7 and inhibit the deacetylation of histone proteins in order to detect the effects of SAHA on MCF-7 cells. Wound healing assays and transwell assays showed that SAHA inhibited the migration of MCF-7 cells. Western blot assays proved that SAHA inhibited the expression of migration-related gene MYL9. MTT assays and colony forming assays demonstrated that SAHA inhibited the proliferation of MCF-7 cells. Western blot assays and RT-qPCR assays proved SAHA inhibited the expression of cell cycle marker genes CyclinD1 and CDK4 and promoted the expression of CDK inhibitor p21.
作者 姚海淋 霍丽红 郝云鹏 来永巍 段慧鑫 欧国芳 何红鹏 YAO Hailin;HUO Lihong;HAO Yunpeng;LAI Yongwei;DUAN Huixin;OU Guofang;HE Hongpeng(Tianjin Key Laboratory of Industrial Microbiology,College of Biotechnology,Tianjin University of Science & Technology,Tianjin 300457,China)
出处 《天津科技大学学报》 CAS 2019年第2期25-29,44,共6页 Journal of Tianjin University of Science & Technology
基金 国家自然基金青年基金资助项目(31301073)
关键词 乳腺癌 MCF-7 细胞 SAHA 细胞增殖 细胞迁移 breast cancer MCF-7 cells SAHA cell proliferation cell migration
  • 相关文献

参考文献3

二级参考文献42

  • 1严冬翔,刘增路,毛振民.多发性骨髓瘤治疗药物研究进展[J].中国药房,2007,18(2):143-146. 被引量:7
  • 2Grunstein M. Histone acetylation inchromatin structure and transcription[J]. Nature, 1997,389:349-352.
  • 3Bronell JE, Zhou J, Ranalli T, et al. Tetrahymena histone acetyltransferase A: ahomolog to yeast Gcn5p linking histone acetylation to gene activation[J].Cell,1996,84:843-851.
  • 4Ogryzko W, Schiltz RL, Rusanova V, et al. The transcriptional coactivators p300 andCBP are histone acetyltransfeases[J].Cell,1996,87:953-959.
  • 5Mizzen CA, Yang Y, Dai P, et al. The TAF250 subunit of TFⅡD has histoneacetyltransferase activity[J]. Cell, 1996,87:1261-1270.
  • 6Chen H, Lin RJ, Schiltz RL, et al. Nuclear receptor coactivator ACTR is a novelhistone acetyltransferase and forms a multimeric activation complex with P/CAF andCBP/p300[J].Cell,1997,90:569-580.
  • 7Li H,Gomes PJ,Chen JD.RAC3, a steroid/nuclear receptor-associated coactivator thatis related to SRC-1 and TIF2[J]. Proc Natl Acad Sci USA, 1997,94:8479-8484.
  • 8Hilfiker A,Hilfiker-Kleiner D,Pannuti A, et al. Mof, a putative acetyltransferasegene related to the Tip 60 and MOZ human genes and to the SAS genes of yeast, is requiredfor dosage compensation in Drosopila[J].EMBO J,1998,17:2886-2893.
  • 9Dutnal RN,Tafrov ST,Sternglanz R,et al.Structure of the histone acetyltransferseHat1: a paradigm for the GCN5-related N-acetyltransferasesuperfamily[J].Cell,1998,94:427-438.
  • 10Imhof A, Yang XJ, Ogryzko Q,et al. Acetylation of general transcription factors byhistone acetyltransferases[J]. Curr Biol,1997,7:689-692.

共引文献9

同被引文献6

引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部