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  1. AU="Paget-Bailly, Philippe"
  2. AU="Rory J McCrimmon"
  3. AU="Ahdoot, Aaron I."
  4. AU="Neote, Kuldeep S"
  5. AU="Shen, Congcong"
  6. AU="Rahi, Kosar"
  7. AU="Channabasavaiah, Jagadish Puralae"
  8. AU="Anselmi, Maurizio"
  9. AU="Chauhan, D."
  10. AU="Nicoll, Roger A"
  11. AU="Kwon, Young-Sam"
  12. AU="Mihwa Lee"
  13. AU="Yuanting Jin"
  14. AU="Ter Haar, Eva"
  15. AU="Wolin, Dan L"
  16. AU="Zhang, Tenan"
  17. AU="Piedrafita, Lídia"
  18. AU="Nandy, Ananya"
  19. AU="Bansemer, Sven"
  20. AU="Kochetov, O"
  21. AU="Liu, Fen"

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  1. Artikel ; Online: The exon junction complex core factor eIF4A3 is a key regulator of HPV16 gene expression.

    Meznad, Koceila / Paget-Bailly, Philippe / Jacquin, Elise / Peigney, Anne / Aubin, François / Guittaut, Michaël / Mougin, Christiane / Prétet, Jean-Luc / Baguet, Aurélie

    Bioscience reports

    2021  Band 41, Heft 4

    Abstract: High-risk human papillomavirus (hrHPVs), particularly HPV16 and HPV18, are the etiologic factors of ano-genital cancers and some head and neck squamous cell carcinomas (HNSCCs). Viral E6 and E7 oncoproteins, controlled at both transcriptional and post- ... ...

    Abstract High-risk human papillomavirus (hrHPVs), particularly HPV16 and HPV18, are the etiologic factors of ano-genital cancers and some head and neck squamous cell carcinomas (HNSCCs). Viral E6 and E7 oncoproteins, controlled at both transcriptional and post-transcriptional levels, drive hrHPVs-induced carcinogenesis. In the present study, we investigated the implication of the DEAD-box helicase eukaryotic translation initiation factor 4A3 (eIF4A3,) an Exon Junction Complex factor, in the regulation of HPV16 gene expression. Our data revealed that the depletion of the factor eIF4A3 up-regulated E7 oncoprotein levels. We also showed that the inhibition of the nonsense-mediated RNA decay (NMD) pathway, resulted in the up-regulation of E7 at both RNA and protein levels. We therefore proposed that HPV16 transcripts might present different susceptibilities to NMD and that this pathway could play a key role in the levels of expression of these viral oncoproteins during the development of HPV-related cancers.
    Mesh-Begriff(e) Cell Line, Tumor ; DEAD-box RNA Helicases/metabolism ; Eukaryotic Initiation Factor-4A/metabolism ; Host-Pathogen Interactions ; Human papillomavirus 16/genetics ; Human papillomavirus 16/metabolism ; Humans ; Papillomavirus E7 Proteins/genetics ; Papillomavirus E7 Proteins/metabolism
    Chemische Substanzen Papillomavirus E7 Proteins ; oncogene protein E7, Human papillomavirus type 16 ; Eukaryotic Initiation Factor-4A (EC 2.7.7.-) ; EIF4A3 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
    Sprache Englisch
    Erscheinungsdatum 2021-03-24
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 764946-0
    ISSN 1573-4935 ; 0144-8463
    ISSN (online) 1573-4935
    ISSN 0144-8463
    DOI 10.1042/BSR20203488
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Comparative RNA sequencing reveals that HPV16 E6 abrogates the effect of E6*I on ROS metabolism.

    Paget-Bailly, Philippe / Meznad, Koceila / Bruyère, Diane / Perrard, Jérôme / Herfs, Michael / Jung, Alain C / Mougin, Christiane / Prétet, Jean-Luc / Baguet, Aurélie

    Scientific reports

    2019  Band 9, Heft 1, Seite(n) 5938

    Abstract: High-risk Human Papillomavirus infections are responsible for anogenital and oropharyngeal cancers. Alternative splicing is an important mechanism controlling HPV16 gene expression. Modulation in the splice pattern leads to polycistronic HPV16 early ... ...

    Abstract High-risk Human Papillomavirus infections are responsible for anogenital and oropharyngeal cancers. Alternative splicing is an important mechanism controlling HPV16 gene expression. Modulation in the splice pattern leads to polycistronic HPV16 early transcripts encoding a full length E6 oncoprotein or truncated E6 proteins, commonly named E6*. Spliced E6*I transcripts are the most abundant RNAs produced in HPV-related cancers. To date, the biological function of the E6*I isoform remains controversial. In this study, we identified, by RNA sequencing, cellular targets deregulated by E6*I, among which genes related to ROS metabolism. Concomitantly, E6*I-overexpressing cells display high levels of ROS. However, co-overexpression of both E6 and E6*I has no effect on ROS production. In HPV16-infected cells expressing different E6/E6*I levels, we show that the newly identified targets CCL2 and RAC2 are increased by E6*I but decreased by E6 expression, suggesting that E6 abrogates the effect of E6*I. Taken together, these data support the idea that E6*I acts independently of E6 to increase ROS production and that E6 has the ability to counteract the effects of E6*I. This asks the question of how E6*I can be considered separately of E6 in the natural history of HPV16 infection.
    Mesh-Begriff(e) Alternative Splicing ; Bone Neoplasms/epidemiology ; Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Bone Neoplasms/virology ; Female ; Host-Pathogen Interactions/genetics ; Human papillomavirus 16/isolation & purification ; Humans ; Oncogene Proteins, Viral/genetics ; Osteosarcoma/epidemiology ; Osteosarcoma/genetics ; Osteosarcoma/pathology ; Osteosarcoma/virology ; Papillomavirus Infections/genetics ; Papillomavirus Infections/pathology ; Papillomavirus Infections/virology ; Reactive Oxygen Species/metabolism ; Repressor Proteins/genetics ; Sequence Analysis, RNA/methods ; Tumor Cells, Cultured ; Uterine Cervical Neoplasms/epidemiology ; Uterine Cervical Neoplasms/genetics ; Uterine Cervical Neoplasms/pathology ; Uterine Cervical Neoplasms/virology
    Chemische Substanzen E6 protein, Human papillomavirus type 16 ; Oncogene Proteins, Viral ; Reactive Oxygen Species ; Repressor Proteins
    Sprache Englisch
    Erscheinungsdatum 2019-04-11
    Erscheinungsland England
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-42393-6
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel: DNA demethylation agent 5azadC downregulates HPV16 E6 expression in cervical cancer cell lines independently of TBX2 expression.

    Perrard, Jerome / Morel, Adrien / Meznad, Koceila / Paget-Bailly, Philippe / Dalstein, Veronique / Guenat, David / Mourareau, Celine / Clavel, Christine / Fauconnet, Sylvie / Baguet, Aurelie / Mougin, Christiane / Pretet, Jean-Luc

    Oncology letters

    2019  Band 19, Heft 1, Seite(n) 1074–1081

    Abstract: HPV16 is the most carcinogenic human papillomavirus and causes >50% of cervical cancers, the majority of anal cancers and 30% of oropharyngeal squamous cell carcinomas. HPV carcinogenesis relies on the continuous expression of the two main viral ... ...

    Abstract HPV16 is the most carcinogenic human papillomavirus and causes >50% of cervical cancers, the majority of anal cancers and 30% of oropharyngeal squamous cell carcinomas. HPV carcinogenesis relies on the continuous expression of the two main viral oncoproteins E6 and E7 that target >150 cellular proteins. Among them, epigenetic modifiers, including DNA Methyl Transferases (DNMT), are dysregulated, promoting an aberrant methylation pattern in HPV-positive cancer cells. It has been previously reported that the treatment of HPV-positive cervical cancer cells with DNMT inhibitor 5-aza-2'-deoxycytidine (5azadC) caused the downregulation of E6 expression due to mRNA destabilization that was mediated by miR-375. Recently, the T-box transcription factor 2 (TBX2) has been demonstrated to repress HPV LCR activity. In the current study, the role of TBX2 in E6 repression was investigated in HPV16 cervical cancer cell lines following 5azadC treatment. A decrease of E6 expression was accompanied by p53 and p21 restoration. While TBX2 mRNA was upregulated in 5azadC-treated SiHa and Ca Ski cells, TBX2 protein was not detectable. Furthermore, the overexpression of TBX2 protein in cervical cancer cells did not allow the repression of E6 expression. The TBX2 transcription factor is therefore unlikely to be associated with the repression of E6 following 5azadC treatment of SiHa and Ca Ski cells.
    Sprache Englisch
    Erscheinungsdatum 2019-11-28
    Erscheinungsland Greece
    Dokumenttyp Journal Article
    ZDB-ID 2573196-8
    ISSN 1792-1082 ; 1792-1074
    ISSN (online) 1792-1082
    ISSN 1792-1074
    DOI 10.3892/ol.2019.11158
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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