Research article summary (published 30 Oct 2009):

Overexpression of Sp1 leads to p53-dependent apoptosis in cancer cells.

Full Abstract

Numerous studies have documented that Sp1 expression level were elevated in various human cancers. However, the promoters of many pro-apoptotic genes have been found to contain the Sp1 binding elements and are activated by Sp1 overexpression. To better understand the role and the mechanism of increased Sp1 levels on apoptosis, we used adenovirus to ectopically express GFP-Sp1 protein in various cancer cell lines. First, in HeLa and A549 cells, we found that Sp1 overexpression suppressed the cell growth and increased the detection of sub-G1 fraction, caspase-3 cleavage, and annexin-V signal revealed that apoptosis occurred. Furthermore, when cells entered the mitotic stage, the cell apoptosis was induced by Sp1 overexpression through affecting mitotic chromatin packaging. We also verified that p53 protein was accumulated and activated the p53-dependent apoptotic pathways in the wild-type p53 cells but not in the p53-mutated or p53-deleted cell lines when these cells were infected with adeno-GFP-Sp1 virus. In addition, A549 (p53(+/+)) cells could be protected from apoptosis under Sp1 overexpression when p53 was knockdown by p53 shRNA. Finally, H1299 (p53(-/-)) cell viability was significantly inhibited by adeno-GFP-Sp1 virus infection in the expression of p53. In conclusion, p53 was an essential factor for Sp1 overexpression-induced apoptotic cell death in transforming cells. (c) 2009 UICC.

Author information

Author/s: Chuang, Jian-Ying (JY); Wu, Chien-Hsing (CH); Lai, Ming-Derg (MD); Chang, Wen-Chang (WC); Hung, Jan-Jong (JJ);

Affiliation: Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: International journal of cancer. Journal international du cancer (Int J Cancer), published in United States. (Language: eng)

Reference: 2009-Nov; vol 125 (issue 9) : pp 2066-76

Dates: Created 2009/09/03; Completed 2009/09/15;

PMID: 19588484, status: MEDLINE (last retrieval date: 9/15/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Apoptosis Cell Line, Tumor Cell Survival Chromatin - metabolism Cyclin-Dependent Kinase Inhibitor p16 - genetics Cyclin-Dependent Kinase Inhibitor p21 - genetics

Gene Expression Regulation, Neoplastic Humans Neoplasms - pathology Sp1 Transcription Factor - physiology Tumor Suppressor Protein p14ARF - genetics Tumor Suppressor Protein p53 - physiology

Associated Chemicals: CDKN1A protein, human (0) ; Chromatin (0) ; Cyclin-Dependent Kinase Inhibitor p16 (0) ; Cyclin-Dependent Kinase Inhibitor p21 (0) ; Sp1 Transcription Factor (0) ; Tumor Suppressor Protein p14ARF (0) ; Tumor Suppressor Protein p53 (0)

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