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学科主题: 口腔医学
题名:
Acetylated Sp1 inhibits PTEN expression through binding to PTEN core promoter and recruitment of HDAC1 and promotes cancer cell migration and invasion
作者: Kou, Xiao-Xing1,2; Hao, Ting2; Meng, Zhen2; Zhou, Yan-Heng1; Gan, Ye-Hua2
刊名: CARCINOGENESIS
发表日期: 2013
DOI: 10.1093/carcin/bgs336
卷: 34, 期:1, 页:58-67
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Oncology
研究领域[WOS]: Oncology
关键词[WOS]: HISTONE DEACETYLASE INHIBITOR ; TUMOR-SUPPRESSOR GENE ; TRANSCRIPTION FACTOR ; GROWTH-FACTOR ; UP-REGULATION ; REPRESS TRANSCRIPTION ; RECEPTOR EXPRESSION ; EPITHELIAL-CELLS ; PROSTATE-CANCER ; ACTIVATION
英文摘要:

Specificity protein 1 (Sp1) is often overexpressed in cancer cells. Its binding sites are known to exist in the phosphatase and tension homolog deleted on chromosome 10 (PTEN) promoter. In this study, we hypothesized that Sp1 negatively regulates PTEN expression. We used several cell lines to determine the effects of Sp1. The results showed that Sp1 overexpression inhibited the expression and promoter activity of PTEN and correspondingly upregulated AKT phosphorylation, whereas Sp1 knockdown upregulated the expression and promoter ability of PTEN and downregulated AKT phosphorylation. Moreover, a series of deletion and site-directed mutations of the PTEN promoter indicated that Sp1 can inhibit PTEN promoter activity through a specific Sp1-binding site at the PTEN core promoter in vivo. Meanwhile, non-acetylated Sp1, with its loss of DNA binding activity, failed to inhibit the expression and promoter activity of PTEN. Histone deacetylase 1 was necessary for Sp1 to inhibit PTEN expression. The inverse expression of Sp1 and PTEN was found in tongue cancer cells and salivary adenoid cystic cancer (SACC)-LM cells (possessing higher potential for lung metastasis than SACC-83) as compared with that in adjacent normal tissue and SACC-83 cells, respectively. Sp1 knockdown decreased the migration and invasion of SACC-LM cells, whereas Sp1 overexpression increased the migration and invasion of SACC-83 cells. Overall, these results suggest that Sp1 is involved in the development and invasiveness of cancer through inhibition of PTEN.

语种: 英语
所属项目编号: 2006-331 ; 81070849
项目资助者: Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry ; National Natural Science Foundation of China
WOS记录号: WOS:000313128600008
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63951
Appears in Collections:北京大学口腔医学院_牙周科_期刊论文

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作者单位: 1.Peking Univ, Dept Orthodont, Sch & Hosp Stomatol, Beijing 100081, Peoples R China
2.Peking Univ, Cent Lab, Sch & Hosp Stomatol, Beijing 100081, Peoples R China

Recommended Citation:
Kou, Xiao-Xing,Hao, Ting,Meng, Zhen,et al. Acetylated Sp1 inhibits PTEN expression through binding to PTEN core promoter and recruitment of HDAC1 and promotes cancer cell migration and invasion[J]. CARCINOGENESIS,2013,34(1):58-67.
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