IR@PKUHSC  > 北京大学临床肿瘤学院  > 病因研究室
学科主题临床医学
Polycomb CBX7 Directly Controls Trimethylation of Histone H3 at Lysine 9 at the p16 Locus
Li, Qiang1; Wang, Xiuhong1; Lu, Zheming1; Zhang, Baozhen1; Guan, Zhenpo1; Liu, Zhaojun1; Zhong, Qiming1; Gu, Liankun1; Zhou, Jing1; Zhu, Budong2; Ji, Jiafu3; Deng, Dajun1
刊名PLOS ONE
2010-10-29
DOI10.1371/journal.pone.0013732
5期:10
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]TUMOR-SUPPRESSOR ; CHROMOBOX PROTEIN ; GENE-EXPRESSION ; INK4A-ARF LOCUS ; DNA METHYLATION ; HUMAN CANCERS ; CELLS ; ISLAND ; HETEROCHROMATIN ; PROGRESSION
英文摘要

Background: H3K9 trimethylation (H3K9me3) and binding of PcG repressor complex-1 (PRC1) may play crucial roles in the epigenetic silencing of the p16 gene. However, the mechanism of the initiation of this trimethylation is unknown.

Methodology/Principal Findings: In the present study, we found that upregulating the expression of PRC1 component Cbx7 in gastric cancer cell lines MGC803 and BGC823 led to significantly suppress the expression of genes within the p16-Arf-p15 locus. H3K9me3 formation was observed at the p16 promoter and Regulatory Domain (RD). CBX7 and SUV39H2 binding to these regions were also detectable in the CBX7-stably upregulated cells. CBX7-SUV39H2 complexes were observed within nucleus in bimolecular fluorescence complementation assay (BiFC). Mutations of the chromodomain or deletion of Pc-box abolished the CBX7-binding and H3K9me3 formation, and thus partially repressed the function of CBX7. SiRNA-knockdown of Suv39h2 blocked the repressive effect of CBX7 on p16 transcription. Moreover, we found that expression of CBX7 in gastric carcinoma tissues with p16 methylation was significantly lower than that in their corresponding normal tissues, which showed a negative correlation with transcription of p16 in gastric mucosa.

Conclusion/Significance: These results demonstrated for the first time, to our knowledge, that CBX7 could initiate H3K9me3 formation at the p16 promoter.

语种英语
WOS记录号WOS:000283645300013
Citation statistics
Cited Times:16[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/55415
Collection北京大学临床肿瘤学院_病因研究室
北京大学第一临床医学院_整形烧伤外科
北京大学临床肿瘤学院_胃肠肿瘤中心一病区
北京大学临床肿瘤学院_乳腺肿瘤内科
北京大学临床肿瘤学院_病因学研究室
作者单位1.Peking Univ, Canc Hosp & Inst, Dept Etiol, Key Lab Carcinogenesis & Translat Res,Minist Educ, Beijing 100871, Peoples R China
2.Peking Univ, Canc Hosp & Inst, Dept Internal Med, Beijing 100871, Peoples R China
3.Peking Univ, Canc Hosp & Inst, Dept Surg, Beijing 100871, Peoples R China
Recommended Citation
GB/T 7714
Li, Qiang,Wang, Xiuhong,Lu, Zheming,et al. Polycomb CBX7 Directly Controls Trimethylation of Histone H3 at Lysine 9 at the p16 Locus[J]. PLOS ONE,2010,5(10).
APA Li, Qiang.,Wang, Xiuhong.,Lu, Zheming.,Zhang, Baozhen.,Guan, Zhenpo.,...&Deng, Dajun.(2010).Polycomb CBX7 Directly Controls Trimethylation of Histone H3 at Lysine 9 at the p16 Locus.PLOS ONE,5(10).
MLA Li, Qiang,et al."Polycomb CBX7 Directly Controls Trimethylation of Histone H3 at Lysine 9 at the p16 Locus".PLOS ONE 5.10(2010).
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