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Sp1 binds to the external promoter of the p73 gene and induces the expression of TAp73gamma in lung cancer
Stella Logotheti, Ioannis Michalopoulos, Maria Sideridou, Alexandros Daskalos, Sophia Kossida, Demetrios A. Spandidos, John K. Field, Borek Vojtesek, Triantafyllos Liloglou, Vassilis Gorgoulis, Vassilis Zoumpourlis
Language English Country England, Great Britain
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MZ0
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from 2005 to 1 year ago
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from 2005-01-01 to 1 year ago
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from 1967-01-01 to 2012-12-31
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- MeSH
- DNA-Binding Proteins * genetics metabolism MeSH
- DNA chemistry metabolism MeSH
- Down-Regulation genetics MeSH
- Nuclear Proteins * genetics metabolism MeSH
- Conserved Sequence genetics MeSH
- Humans MeSH
- RNA, Small Interfering genetics MeSH
- Plicamycin analogs & derivatives pharmacology MeSH
- Molecular Sequence Data MeSH
- Cell Line, Tumor MeSH
- Tumor Suppressor Proteins * genetics metabolism MeSH
- Lung Neoplasms * metabolism MeSH
- Oligodeoxyribonucleotides genetics metabolism MeSH
- Promoter Regions, Genetic * genetics MeSH
- Protein Isoforms * genetics metabolism MeSH
- Electrophoretic Mobility Shift Assay MeSH
- Base Sequence genetics MeSH
- Sp1 Transcription Factor * antagonists & inhibitors genetics metabolism MeSH
- Vascular Endothelial Growth Factor A metabolism MeSH
- Protein Binding genetics MeSH
- Binding Sites genetics MeSH
- Computational Biology MeSH
- Check Tag
- Humans MeSH
The p73 gene possesses an extrinsic P1 promoter and an intrinsic P2 promoter, resulting in TAp73 and DeltaNup73 isoforms, respectively. The ultimate effect of p73 in oncogenesis is thought to depend on the apoptotic TA to antiapoptotic DeltaN isoforms' ratio. This study was aimed at identifying novel transcription factors that affect TA isoform synthesis. With the use of bioinformatics tools, in vitro binding assays, and chromatin immunoprecipitation analysis, a region extending -233 to -204 bp upstream of the transcription start site of the human p73 P1 promoter, containing conserved Sp1-binding sites, was characterized. Treatment of cells with Sp1 RNAi and Sp1 inhibitor functionally suppress TAp73 expression, indicating positive regulation of P1 by the Sp1 protein. Notably Sp1 inhibition or knockdown also reduces DeltaNup73 protein levels. Therefore, Sp1 directly regulates TAp73 transcription and affects DeltaNup73 levels in lung cancer. TAp73gamma was shown to be the only TA isoform overexpressed in several lung cancer cell lines and in 26 non-small cell lung cancers, consistent with Sp1 overexpression, thereby questioning the apoptotic role of this specific p73 isoform in lung cancer.
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- $a The p73 gene possesses an extrinsic P1 promoter and an intrinsic P2 promoter, resulting in TAp73 and DeltaNup73 isoforms, respectively. The ultimate effect of p73 in oncogenesis is thought to depend on the apoptotic TA to antiapoptotic DeltaN isoforms' ratio. This study was aimed at identifying novel transcription factors that affect TA isoform synthesis. With the use of bioinformatics tools, in vitro binding assays, and chromatin immunoprecipitation analysis, a region extending -233 to -204 bp upstream of the transcription start site of the human p73 P1 promoter, containing conserved Sp1-binding sites, was characterized. Treatment of cells with Sp1 RNAi and Sp1 inhibitor functionally suppress TAp73 expression, indicating positive regulation of P1 by the Sp1 protein. Notably Sp1 inhibition or knockdown also reduces DeltaNup73 protein levels. Therefore, Sp1 directly regulates TAp73 transcription and affects DeltaNup73 levels in lung cancer. TAp73gamma was shown to be the only TA isoform overexpressed in several lung cancer cell lines and in 26 non-small cell lung cancers, consistent with Sp1 overexpression, thereby questioning the apoptotic role of this specific p73 isoform in lung cancer.
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