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EFFECT OFZEB1 OVEREXPRESSION AND SILENCING ON AN ER-A PROMOTER OF METHY LATION OF BREAST CANCER CELLS AND THE MECHANISM OF ITS TRANSCRIPTIONAL INHIBITION

文献类型：期刊论文

作者Li, Yongfeng2,3; Rui, Xinmiao4; Chen, Daobao2,3; Zou, Dehong2,3; Meng, Xuli1
刊名ACTA MEDICA MEDITERRANEA
出版日期2021
卷号37
关键词ZEB1 breast cancer DNMT3B HDAC1
ISSN号0393-6384
DOI10.19193/0393-6384_2021_4_328
通讯作者Meng, Xuli(munff8@163.com)
英文摘要Objective: To investigate the effect of zinc finger E-box binding homeobox 1 (ZEB1) overexpression and silencing on the estrogen receptor-alpha (ER-alpha) promoter methylation of breast cancer cells and the mechanism of its transcription inhibition. Methods: MDA-MB-231 cell lines were randomly divided into a Ctrl group, an AZA group, a VPA group and an AZA+VPA group. MCF-7 cell lines were selected and randomly divided into a Ctrl group, ZEB1 group, AZA group, VPA group, and AZA+VPA group. The mRNA and protein expression levels of ZEB1 and ER-a in breast cancer cell lines were compared. The expression of DNMT3B and HDAC1 in each group was compared. Results: The expression levels of ZEB1 decreased and the expression levels of ER-alpha increased. The expression levels of mRNA and ZEB1 proteins in the cells were significantly lower, but the expression levels of ER-alpha mRNA and proteins in the cells were significantly higher in the h-ZEB1-MDA-MAB-231 group than those in the SC-MDA-MAB-231 group (P<0.05). Moreover, ZEB1 could simultaneously precipitate DNMT3B and HDAC1 proteins, and DNMT3B and HDAC1 antibodies could also correspondingly precipitate ZEB1 protein expression, suggesting that the combination of ZEB1, DNMT3B, and HDAC1 can produce a protein complex. DNMT3B and HDAC1 can also be enriched in the sequence region of E2box elements. Conclusions: ZEB1 can induce the hypermethylation of an ER-alpha promoter in breast cancer cells and its mechanism may be achieved by recruiting DNMT3B and HDAC1 to the ER-alpha promoter region.
资助项目Natural Science Foundation of Zhejiang Province[LQ17H160013] ; Zhejiang Province Health Department Foundation[2018ky284]
WOS研究方向General & Internal Medicine
语种英语
WOS记录号WOS:000673269100028
出版者CARBONE EDITORE
资助机构Natural Science Foundation of Zhejiang Province ; Zhejiang Province Health Department Foundation
源URL[http://ir.hfcas.ac.cn:8080/handle/334002/123114]  
专题中国科学院合肥物质科学研究院
通讯作者Meng, Xuli
作者单位1.Zhejiang Prov Peoples Hosp, Dept Breast Surg, Hangzhou 310022, Peoples R China
2.Univ Chinese Acad Sci, Canc Hosp, Zhejiang Canc Hosp, Dept Breast Surg, Hangzhou 310022, Peoples R China
3.Chinese Acad Sci, Inst Canc & Basic Med IBMC, Hangzhou 310022, Peoples R China
4.Zhejiang Chinese Med Univ, Clin Med Coll 2, Hangzhou 310022, Peoples R China
推荐引用方式
GB/T 7714		 Li, Yongfeng,Rui, Xinmiao,Chen, Daobao,et al. EFFECT OFZEB1 OVEREXPRESSION AND SILENCING ON AN ER-A PROMOTER OF METHY LATION OF BREAST CANCER CELLS AND THE MECHANISM OF ITS TRANSCRIPTIONAL INHIBITION[J]. ACTA MEDICA MEDITERRANEA,2021,37.
APA Li, Yongfeng,Rui, Xinmiao,Chen, Daobao,Zou, Dehong,&Meng, Xuli.(2021).EFFECT OFZEB1 OVEREXPRESSION AND SILENCING ON AN ER-A PROMOTER OF METHY LATION OF BREAST CANCER CELLS AND THE MECHANISM OF ITS TRANSCRIPTIONAL INHIBITION.ACTA MEDICA MEDITERRANEA,37.
MLA Li, Yongfeng,et al."EFFECT OFZEB1 OVEREXPRESSION AND SILENCING ON AN ER-A PROMOTER OF METHY LATION OF BREAST CANCER CELLS AND THE MECHANISM OF ITS TRANSCRIPTIONAL INHIBITION".ACTA MEDICA MEDITERRANEA 37(2021).

入库方式： OAI收割

来源：合肥物质科学研究院

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