Trail is a key target in S-phase slowing-dependent apoptosis induced by interferon-beta in cervical carcinoma cells. (Articolo in rivista)

Type

• Prodotto della ricerca (Classe)
• Articolo in rivista (Classe)

Label

• Trail is a key target in S-phase slowing-dependent apoptosis induced by interferon-beta in cervical carcinoma cells. (Articolo in rivista) (literal)

Anno

• 2005-01-01T00:00:00+01:00 (literal)

Alternative label

• Serena Vannucchi; Maria vincenza Chiantore; Gianna Fiorucci; Zulema Antonia Percario; Stefano Leone; Elisabetta Affabris; Giovanna Romeo. (2005)
  Trail is a key target in S-phase slowing-dependent apoptosis induced by interferon-beta in cervical carcinoma cells.
  in Oncogene (Basingstoke)
  (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

• Serena Vannucchi; Maria vincenza Chiantore; Gianna Fiorucci; Zulema Antonia Percario; Stefano Leone; Elisabetta Affabris; Giovanna Romeo. (literal)

Pagina inizio

• 2536 (literal)

Pagina fine

• 2546 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

• 24 (literal)

Rivista

• Oncogene (Rivista)

Note

• ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

• S.V., M.V.C., Istituto Superiore di Sanità; Z.A.P., S.L., E.A. Università Roma Tre (literal)

Titolo

• Trail is a key target in S-phase slowing-dependent apoptosis induced by interferon-beta in cervical carcinoma cells. (literal)

Abstract

• Interferon (IFN)-beta induces S-phase slowing and apoptosis in human papilloma virus (HPV)-positive cervical carcinoma cell line ME-180. Here, we show that apoptosis is a consequence of the S-phase lengthening imposed by IFN-beta, demonstrating the functional correlation between S-phase alteration and apoptosis induction. In ME-180 cells, where p53 function is inhibited by HPV E6 oncoprotein, IFN-beta effects on cell cycle and apoptosis occur independently of p53. The apoptosis due to IFN-beta is mediated by the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in a manner dependent on the S-phase deregulation. IFN-beta appears to increase TRAIL expression both directly at the mRNA level and indirectly by augmenting surface protein levels as a consequence of the induced S-phase cell accumulation. Moreover, the alteration of the S-phase due to IFN-beta promotes TRAIL-dependent apoptosis by potentiating cell sensitivity to TRAIL, possibly through induction of a proapoptotic NF-kappaB activity and TRAIL-R2 receptor expression. Interestingly, IFN-beta-induced TRAIL-dependent apoptotic events strongly differ in the requirement of caspase activity. These results show that IFN-beta may induce an apoptotic response by deregulating cell cycle. Understanding the linkage between these mechanisms appears to be of primary importance in the search for new IFN-based therapeutic strategies to circumvent cancer disease or improve clinical outcome. (literal)

Prodotto di

• Controllo di proliferazione, differenziamento e morte cellulare (SV.P15.010.001) (Modulo)
• Institute of molecular biology and pathology (IBPM) (Istituto)

Autore CNR

• GIOVANNA ROMEO (Persona)
• GIANNA FIORUCCI (Persona)

Incoming links:

Prodotto

• Institute of molecular biology and pathology (IBPM) (Istituto)
• Controllo di proliferazione, differenziamento e morte cellulare (SV.P15.010.001) (Modulo)

Autore CNR di

• GIANNA FIORUCCI (Persona)
• GIOVANNA ROMEO (Persona)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#rivistaDi

• Oncogene (Rivista)