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  • 1
    Keywords: GENE ; transcription ; ACID ; ACIDS ; p53 ; RE ; MCP-1
    Type of Publication: Journal article epub ahead of print
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  • 2
    Keywords: CANCER ; CANCER CELLS ; CELLS ; EXPRESSION ; carcinoma ; Germany ; KINASE ; PROTEIN ; RNA ; transcription ; COMPLEX ; COMPLEXES ; AP-1 ; PROTEIN-KINASE ; CHROMATIN ; ASSAY ; c-Fos ; CARCINOMA CELLS ; PROMOTER ; CERVICAL-CANCER ; CANCER-CELLS ; MAMMALIAN-CELLS ; TRANSFORMATION ; CERVICAL-CARCINOMA ; BINDS ; C-FOS EXPRESSION ; BINDING PROTEIN ; SERUM ; MALIGNANT-CELLS ; targeted ; KINASE PATHWAY ; SIGNAL-TRANSDUCTION PATHWAYS ; TERNARY COMPLEX ; C-FOS PROMOTER ; ASSAYS ; REPRESSOR ; KINASE-ACTIVITY ; AP-1 TRANSCRIPTION ; HUMAN-PAPILLOMAVIRUS TRANSCRIPTION ; SELECTIVE SUPPRESSION ; SERUM RESPONSE ELEMENT
    Abstract: We have investigated the expression of c-fos in cervical carcinoma cells and in somatic cell hybrids derived therefrom. In malignant cells, c-fos was constitutively expressed even after serum starvation. Dissection of the c-fos promoter showed that expression was mainly controlled by the SRE motif, which was active in malignant cells, but repressed in their non-malignant counterparts. Constitutive SRE activity was not mediated by sustained mitogen-activated protein kinase activity but because of inefficient expression of the ternary complex factor Net, which was either very low or even barely discernible. Chromatin immunoprecipitation assays revealed that Net directly binds to the SRE nucleoprotein complex in non-tumorigenic cells, but not in malignant segregants. Small interfering RNA targeted against Net resulted in enhanced c-fos transcription, clearly illustrating its repressor function. Conversely, stable ectopic expression of Net in malignant cells negatively regulated endogenous c-fos, resulting in a disappearance of the c-Fos protein from the AP-1 transcription complex. These data indicate that loss of Net and constitutive c-fos expression appear to be a key event in the transformation of cervical cancer cells
    Type of Publication: Journal article published
    PubMed ID: 15548518
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  • 3
    Keywords: CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; CELL ; Germany ; IN-VIVO ; VITRO ; VIVO ; PROTEIN ; transcription ; NF-KAPPA-B ; TUMOR-NECROSIS-FACTOR ; ACTIVATION ; CARCINOGENESIS ; KERATINOCYTES ; BINDING ; BIOLOGY ; papillomavirus ; CHROMATIN ; ASSAY ; MUTATION ; inactivation ; p53 ; REGION ; human papillomavirus ; SURVEILLANCE ; CERVICAL-CARCINOMA CELLS ; E6 ; HUMAN KERATINOCYTES ; ONCOPROTEIN ; TNF-ALPHA ; ONCOLOGY ; SIRNA ; Lead ; IMMUNE ; CANCER SYNDROME ; CHEMOATTRACTANT PROTEIN-1 GENE ; JE GENE ; SUPPRESSOR P53
    Abstract: Background: Our previous studies showed that the expression of the monocyte-chemoattractant protein (MCP)-1, a chemokine, which triggers the infiltration and activation of cells of the monocyte-macrophage lineage, is abrogated in human papillomavirus (HPV)-positive premalignant and malignant cells. In silico analysis of the MCP-1 upstream region proposed a putative p53 binding side about 2.5 kb upstream of the transcriptional start. The aim of this study is to monitor a physiological role of p53 in this process. Results: The proposed p53 binding side could be confirmed in vitro by electrophoretic-mobility-shift assays and in vivo by chromatin immunoprecipitation. Moreover, the availability of p53 is apparently important for chemokine regulation, since TNF-alpha can induce MCP-1 only in human keratinocytes expressing the viral oncoprotein E7, but not in HPV16 E6 positive cells, where p53 becomes degraded. A general physiological role of p53 in MCP-1 regulation was further substantiated in HPV-negative cells harboring a temperature-sensitive mutant of p53 and in Li-Fraumeni cells, carrying a germ-line mutation of p53. In both cases, non-functional p53 leads to diminished MCP-1 transcription upon TNF-alpha treatment. In addition, siRNA directed against p53 decreased MCP-1 transcription after TNF-alpha addition, directly confirming a crosstalk between p53 and MCP-1. Conclusion: These data support the concept that p53 inactivation during carcinogenesis also affects immune surveillance by interfering with chemokine expression and in turn communication with cells of the immunological compartment
    Type of Publication: Journal article published
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