PMID- 19588484
OWN - NLM
STAT- MEDLINE
DCOM- 20090915
LR  - 20220321
IS  - 1097-0215 (Electronic)
IS  - 0020-7136 (Linking)
VI  - 125
IP  - 9
DP  - 2009 Nov 1
TI  - Overexpression of Sp1 leads to p53-dependent apoptosis in cancer cells.
PG  - 2066-76
LID - 10.1002/ijc.24563 [doi]
AB  - 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.
CI  - (c) 2009 UICC.
FAU - Chuang, Jian-Ying
AU  - Chuang JY
AD  - Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung 
      University, Tainan, Taiwan.
FAU - Wu, Chien-Hsing
AU  - Wu CH
FAU - Lai, Ming-Derg
AU  - Lai MD
FAU - Chang, Wen-Chang
AU  - Chang WC
FAU - Hung, Jan-Jong
AU  - Hung JJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (CDKN1A protein, human)
RN  - 0 (Chromatin)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p16)
RN  - 0 (Cyclin-Dependent Kinase Inhibitor p21)
RN  - 0 (Sp1 Transcription Factor)
RN  - 0 (Tumor Suppressor Protein p14ARF)
RN  - 0 (Tumor Suppressor Protein p53)
SB  - IM
MH  - *Apoptosis
MH  - Cell Line, Tumor
MH  - Cell Survival
MH  - Chromatin/metabolism
MH  - Cyclin-Dependent Kinase Inhibitor p16/genetics
MH  - Cyclin-Dependent Kinase Inhibitor p21/genetics
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Neoplasms/*pathology
MH  - Sp1 Transcription Factor/*physiology
MH  - Tumor Suppressor Protein p14ARF/genetics
MH  - Tumor Suppressor Protein p53/*physiology
EDAT- 2009/07/10 09:00
MHDA- 2009/09/16 06:00
CRDT- 2009/07/10 09:00
PHST- 2009/07/10 09:00 [entrez]
PHST- 2009/07/10 09:00 [pubmed]
PHST- 2009/09/16 06:00 [medline]
AID - 10.1002/ijc.24563 [doi]
PST - ppublish
SO  - Int J Cancer. 2009 Nov 1;125(9):2066-76. doi: 10.1002/ijc.24563.