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  1. Article: Yin Yang 1 cooperates with activator protein 2 to stimulate ERBB2 gene expression in mammary cancer cells.

    Begon, Dominique Y / Delacroix, Laurence / Vernimmen, Douglas / Jackers, Pascale / Winkler, Rosita

    The Journal of biological chemistry

    2005  Volume 280, Issue 26, Page(s) 24428–24434

    Abstract: Overexpression of the ERBB2 oncogene is observed in about 30% of breast cancers and is generally correlated with a poor prognosis. Previous results from our and other laboratories indicated that elevated transcriptional activity contributes significantly ...

    Abstract Overexpression of the ERBB2 oncogene is observed in about 30% of breast cancers and is generally correlated with a poor prognosis. Previous results from our and other laboratories indicated that elevated transcriptional activity contributes significantly to the overexpression of ERBB2 mRNA in mammary adenocarcinoma cell lines. Activator protein 2 (AP-2) transcription factors account for this overexpression through two recognition sequences located 215 and 500 bp upstream from the transcription start site. Furthermore, AP-2 transcription factors are highly expressed in cancer cell lines overexpressing ERBB2. In this report, we examined the cooperative effect of Yin Yang 1 (YY1) on AP-2-induced activation of ERBB2 promoter activity. We detected high levels of YY1 transcription factor in mammary cancer cell lines. Notably, we showed that YY1 enhances AP-2alpha transcriptional activation of the ERBB2 promoter through an AP-2 site both in HepG2 and in HCT116 cells, whereas a carboxyl-terminal-truncated form of YY1 cannot. Moreover, we demonstrated the interaction between endogenous AP-2 and YY1 factors in the BT-474 mammary adenocarcinoma cell line. In addition, inhibition of endogenous YY1 protein by an antisense decreased the transcription of an AP-2-responsive ERBB2 reporter plasmid in BT-474 breast cancer cells. Finally, we detected in vivo AP-2 and YY1 occupancy of the ERBB2 proximal promoter in chromatin immunoprecipitation assays. Our data thus provide evidence that YY1 cooperates with AP-2 to stimulate ERBB2 promoter activity through the AP-2 binding sites.
    MeSH term(s) Binding Sites ; Blotting, Western ; Breast Neoplasms/metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus/metabolism ; Chromatin/chemistry ; Chromatin Immunoprecipitation ; DNA-Binding Proteins/metabolism ; DNA-Binding Proteins/physiology ; Erythroid-Specific DNA-Binding Factors ; Gene Expression Regulation, Neoplastic ; Genetic Vectors ; Humans ; Immunoprecipitation ; Luciferases/metabolism ; Models, Genetic ; Oligonucleotides, Antisense/chemistry ; Plasmids/metabolism ; Promoter Regions, Genetic ; Protein Binding ; RNA, Messenger/metabolism ; Receptor, ErbB-2/biosynthesis ; Transcription Factor AP-2 ; Transcription Factors/metabolism ; Transcription Factors/physiology ; Transcription, Genetic ; Transcriptional Activation ; Transfection ; YY1 Transcription Factor
    Chemical Substances Chromatin ; DNA-Binding Proteins ; Erythroid-Specific DNA-Binding Factors ; Oligonucleotides, Antisense ; RNA, Messenger ; TFAP2A protein, human ; Transcription Factor AP-2 ; Transcription Factors ; YY1 Transcription Factor ; YY1 protein, human ; Luciferases (EC 1.13.12.-) ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2005-05-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M503790200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The human epidermal growth factor receptor (EGFR) gene in European patients with advanced colorectal cancer harbors infrequent mutations in its tyrosine kinase domain

    Delvenne Philippe / Boniver Jacques / Pauly Marc / Berchem Guy / Kayser Jacques / Faber Carlo / Begon Dominique Y / Chambeau Laetitia / Metzger Brigitte / Dicato Mario / Wenner Thomas

    BMC Medical Genetics, Vol 12, Iss 1, p

    2011  Volume 144

    Abstract: Abstract Background The epidermal growth factor receptor (EGFR), a member of the ErbB family of receptors, is a transmembrane tyrosine kinase (TK) activated by the binding of extracellular ligands of the EGF-family and involved in triggering the MAPK ... ...

    Abstract Abstract Background The epidermal growth factor receptor (EGFR), a member of the ErbB family of receptors, is a transmembrane tyrosine kinase (TK) activated by the binding of extracellular ligands of the EGF-family and involved in triggering the MAPK signaling pathway, which leads to cell proliferation. Mutations in the EGFR tyrosine kinase domain are frequent in non-small-cell lung cancer (NSCLC). However, to date, only very few, mainly non-European, studies have reported rare EGFR mutations in colorectal cancer (CRC). Methods We screened 236 clinical tumor samples from European patients with advanced CRC by direct DNA sequencing to detect potential, as yet unknown mutations, in the EGFR gene exons 18 to 21, mainly covering the EGFR TK catalytic domain. Results EGFR sequences showed somatic missense mutations in exons 18 and 20 at a frequency of 2.1% and 0.4% respectively. Somatic SNPs were also found in exons 20 and 21 at a frequency of about 3.1% and 0.4% respectively. Of these mutations, four have not yet been described elsewhere. Conclusions These mutation frequencies are higher than in a similarly sized population characterized by Barber and colleagues, but still too low to account for a major role played by the EGFR gene in CRC.
    Keywords Internal medicine ; RC31-1245 ; Genetics ; QH426-470
    Subject code 616
    Language English
    Publishing date 2011-10-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Silencing of E7 oncogene restores functional E-cadherin expression in human papillomavirus 16-transformed keratinocytes.

    Caberg, Jean-Hubert D / Hubert, Pascale M / Begon, Dominique Y / Herfs, Michael F / Roncarati, Patrick J / Boniver, Jacques J / Delvenne, Philippe O

    Carcinogenesis

    2008  Volume 29, Issue 7, Page(s) 1441–1447

    Abstract: Human papillomavirus (HPV) infection, particularly type 16, is causally associated with cancer of the uterine cervix. The persistence or progression of cervical lesions suggests that viral antigens are not adequately presented to the immune system. This ... ...

    Abstract Human papillomavirus (HPV) infection, particularly type 16, is causally associated with cancer of the uterine cervix. The persistence or progression of cervical lesions suggests that viral antigens are not adequately presented to the immune system. This hypothesis is reinforced by the observation that most squamous intra-epithelial lesions show quantitative and functional alterations of Langerhans cells (LCs). Moreover, E-cadherin-dependent adhesion of LC to keratinocytes (KCs) is defective in cervical HPV16-associated (pre)neoplastic lesions. The possible role of viral oncoprotein E7 in the reduced levels of cell surface E-cadherin was investigated by silencing HPV16 E7 by RNA interference (siRNA). This treatment induced an increased cell surface E-cadherin expression in HPV16-positive KC and a significant adhesion of LC to these squamous cells. The E-cadherin re-expression following HPV16 E7 silencing was associated with increased detection levels of retinoblastoma protein and the activating protein (AP)-2alpha transcription factor. These data suggest that HPV16 E7-induced alterations of LC/KC adhesion may play a role in the defective immune response during cervical carcinogenesis.
    MeSH term(s) Antigens, CD1/biosynthesis ; Cadherins/biosynthesis ; Cadherins/genetics ; Carcinoma, Squamous Cell/genetics ; Carcinoma, Squamous Cell/immunology ; Carcinoma, Squamous Cell/pathology ; Carcinoma, Squamous Cell/virology ; Cell Adhesion/genetics ; Cell Line, Tumor ; Cell Transformation, Viral/genetics ; Cell Transformation, Viral/immunology ; Female ; Gene Silencing ; Human papillomavirus 16/genetics ; Humans ; Keratinocytes/immunology ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Keratinocytes/virology ; Langerhans Cells/immunology ; Langerhans Cells/metabolism ; Langerhans Cells/pathology ; Langerhans Cells/virology ; Oncogene Proteins, Viral/biosynthesis ; Oncogene Proteins, Viral/genetics ; Papillomavirus E7 Proteins ; Papillomavirus Infections/genetics ; Papillomavirus Infections/immunology ; Papillomavirus Infections/metabolism ; Papillomavirus Infections/pathology ; RNA Interference ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Transcription Factor AP-2/biosynthesis ; Transcription Factor AP-2/genetics ; Transfection ; Uterine Cervical Neoplasms/genetics ; Uterine Cervical Neoplasms/immunology ; Uterine Cervical Neoplasms/pathology ; Uterine Cervical Neoplasms/virology
    Chemical Substances Antigens, CD1 ; CD1a antigen ; Cadherins ; Oncogene Proteins, Viral ; Papillomavirus E7 Proteins ; RNA, Messenger ; RNA, Small Interfering ; Transcription Factor AP-2 ; oncogene protein E7, Human papillomavirus type 16
    Language English
    Publishing date 2008-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgn145
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1558: Show issues Location:
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  4. Article ; Online: Novel association between vasoactive intestinal peptide and CRTH2 receptor in recruiting eosinophils: a possible biochemical mechanism for allergic eosinophilic inflammation of the airways.

    El-Shazly, Amr E / Begon, Dominique Y / Kustermans, Gaelle / Arafa, Mohammad / Dortu, Estelle / Henket, Monique / Lefebvre, Philippe P / Louis, Renaud / Delvenne, Philippe

    The Journal of biological chemistry

    2012  Volume 288, Issue 2, Page(s) 1374–1384

    Abstract: We explored the relation between vasoactive intestinal peptide (VIP), CRTH2, and eosinophil recruitment. It is shown that CRTH2 expression by eosinophils from allergic rhinitis (AR) patients and eosinophil cell line (Eol-1 cells) was up-regulated by VIP ... ...

    Abstract We explored the relation between vasoactive intestinal peptide (VIP), CRTH2, and eosinophil recruitment. It is shown that CRTH2 expression by eosinophils from allergic rhinitis (AR) patients and eosinophil cell line (Eol-1 cells) was up-regulated by VIP treatment. This was functional and resulted in exaggerated migratory response of cells against PGD2. Nasal challenge of AR patients resulted in a significant increase of VIP contents in nasal secretion (ELISA), and the immunohistochemical studies of allergic nasal tissues showed significant expression of VIP in association with intense eosinophil recruitment. Biochemical assays showed that VIP-induced eosinophil chemotaxis from AR patients and Eol-1 cells was mediated through the CRTH2 receptor. Cell migration against VIP was sensitive to protein kinase C (PKC) and protein kinase A (PKA) inhibition but not to tyrosine kinase or p38 MAPK inhibition or calcium chelation. Western blot demonstrated a novel CRTH2-mediated cytosol-to-membrane translocation of PKC-ε, PKC-δ, and PKA-α, -γ, and -IIαreg in Eol-1 cells upon stimulation with VIP. Confocal images and FACS demonstrated a strong association and co-localization between VIP peptide and CRTH2 molecules. Further, VIP induced PGD2 secretion from eosinophils. Our results demonstrate the first evidence of association between VIP and CRTH2 in recruiting eosinophils.
    MeSH term(s) Amino Acid Sequence ; Base Sequence ; DNA Primers ; Enzyme-Linked Immunosorbent Assay ; Eosinophilia/metabolism ; Eosinophilia/pathology ; Eosinophils/cytology ; Flow Cytometry ; Humans ; Hypersensitivity/metabolism ; Hypersensitivity/pathology ; Immunohistochemistry ; Molecular Sequence Data ; Receptors, Immunologic/metabolism ; Receptors, Prostaglandin/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Trachea/metabolism ; Trachea/pathology ; Vasoactive Intestinal Peptide/chemistry ; Vasoactive Intestinal Peptide/metabolism
    Chemical Substances DNA Primers ; Receptors, Immunologic ; Receptors, Prostaglandin ; Vasoactive Intestinal Peptide (37221-79-7) ; prostaglandin D2 receptor (XZF106QU24)
    Language English
    Publishing date 2012-11-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.M112.422675
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  5. Article ; Online: The human epidermal growth factor receptor (EGFR) gene in European patients with advanced colorectal cancer harbors infrequent mutations in its tyrosine kinase domain.

    Metzger, Brigitte / Chambeau, Laetitia / Begon, Dominique Y / Faber, Carlo / Kayser, Jacques / Berchem, Guy / Pauly, Marc / Boniver, Jacques / Delvenne, Philippe / Dicato, Mario / Wenner, Thomas

    BMC medical genetics

    2011  Volume 12, Page(s) 144

    Abstract: Background: The epidermal growth factor receptor (EGFR), a member of the ErbB family of receptors, is a transmembrane tyrosine kinase (TK) activated by the binding of extracellular ligands of the EGF-family and involved in triggering the MAPK signaling ... ...

    Abstract Background: The epidermal growth factor receptor (EGFR), a member of the ErbB family of receptors, is a transmembrane tyrosine kinase (TK) activated by the binding of extracellular ligands of the EGF-family and involved in triggering the MAPK signaling pathway, which leads to cell proliferation. Mutations in the EGFR tyrosine kinase domain are frequent in non-small-cell lung cancer (NSCLC). However, to date, only very few, mainly non-European, studies have reported rare EGFR mutations in colorectal cancer (CRC).
    Methods: We screened 236 clinical tumor samples from European patients with advanced CRC by direct DNA sequencing to detect potential, as yet unknown mutations, in the EGFR gene exons 18 to 21, mainly covering the EGFR TK catalytic domain.
    Results: EGFR sequences showed somatic missense mutations in exons 18 and 20 at a frequency of 2.1% and 0.4% respectively. Somatic SNPs were also found in exons 20 and 21 at a frequency of about 3.1% and 0.4% respectively. Of these mutations, four have not yet been described elsewhere.
    Conclusions: These mutation frequencies are higher than in a similarly sized population characterized by Barber and colleagues, but still too low to account for a major role played by the EGFR gene in CRC.
    MeSH term(s) Base Sequence ; Colorectal Neoplasms/genetics ; DNA Mutational Analysis ; ErbB Receptors/genetics ; European Continental Ancestry Group/genetics ; Exons ; Gene Frequency ; Humans ; Mutation, Missense/genetics ; Polymorphism, Single Nucleotide ; Protein Structure, Tertiary ; Protein-Tyrosine Kinases/genetics
    Chemical Substances ErbB Receptors (EC 2.7.10.1) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2011-10-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1471-2350
    ISSN (online) 1471-2350
    DOI 10.1186/1471-2350-12-144
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  6. Article ; Online: The combined immunodetection of AP-2alpha and YY1 transcription factors is associated with ERBB2 gene overexpression in primary breast tumors.

    Allouche, Abdelkader / Nolens, Gregory / Tancredi, Annalisa / Delacroix, Laurence / Mardaga, Julie / Fridman, Viviana / Winkler, Rosita / Boniver, Jacques / Delvenne, Philippe / Begon, Dominique Y

    Breast cancer research : BCR

    2008  Volume 10, Issue 1, Page(s) R9

    Abstract: Introduction: Overexpression of the ERBB2 oncogene is observed in about 20% of human breast tumors and is the consequence of increased transcription rates frequently associated with gene amplification. Several studies have shown a link between activator ...

    Abstract Introduction: Overexpression of the ERBB2 oncogene is observed in about 20% of human breast tumors and is the consequence of increased transcription rates frequently associated with gene amplification. Several studies have shown a link between activator protein 2 (AP-2) transcription factors and ERBB2 gene expression in breast cancer cell lines. Moreover, the Yin Yang 1 (YY1) transcription factor has been shown to stimulate AP-2 transcriptional activity on the ERBB2 promoter in vitro. In this report, we examined the relationships between ERBB2, AP-2alpha, and YY1 both in breast cancer tissue specimens and in a mammary cancer cell line.
    Methods: ERBB2, AP-2alpha, and YY1 protein levels were analyzed by immunohistochemistry in a panel of 55 primary breast tumors. ERBB2 gene amplification status was determined by fluorescent in situ hybridization. Correlations were evaluated by a chi2 test at a p value of less than 0.05. The functional role of AP-2alpha and YY1 on ERBB2 gene expression was analyzed by small interfering RNA (siRNA) transfection in the BT-474 mammary cancer cell line followed by real-time reverse transcription-polymerase chain reaction and Western blotting.
    Results: We observed a statistically significant correlation between ERBB2 and AP-2alpha levels in the tumors (p < 0.01). Moreover, associations were found between ERBB2 protein level and the combined high expression of AP-2alpha and YY1 (p < 0.02) as well as between the expression of AP-2alpha and YY1 (p < 0.001). Furthermore, the levels of both AP-2alpha and YY1 proteins were inversely correlated to ERBB2 gene amplification status in the tumors (p < 0.01). Transfection of siRNAs targeting AP-2alpha and AP-2gamma mRNAs in the BT-474 breast cancer cell line repressed the expression of the endogenous ERBB2 gene at both the mRNA and protein levels. Moreover, the additional transfection of an siRNA directed against the YY1 transcript further reduced the ERBB2 protein level, suggesting that AP-2 and YY1 transcription factors cooperate to stimulate the transcription of the ERBB2 gene.
    Conclusion: This study highlights the role of both AP-2alpha and YY1 transcription factors in ERBB2 oncogene overexpression in breast tumors. Our results also suggest that high ERBB2 expression may result either from gene amplification or from increased transcription factor levels.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Cell Line, Tumor ; Female ; Genes, erbB-2/genetics ; Humans ; Immunohistochemistry ; Middle Aged ; Transcription Factor AP-2/biosynthesis ; Transcription Factor AP-2/genetics ; YY1 Transcription Factor/biosynthesis ; YY1 Transcription Factor/genetics
    Chemical Substances Transcription Factor AP-2 ; YY1 Transcription Factor ; YY1 protein, human
    Language English
    Publishing date 2008-01-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2015059-3
    ISSN 1465-542X ; 1465-5411
    ISSN (online) 1465-542X
    ISSN 1465-5411
    DOI 10.1186/bcr1851
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    Zs.A 5494: Show issues Location:
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