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Acquired resistance to oxaliplatin is not directly associated with increased resistance to DNA damage in SK-N-ASrOXALI4000, a newly established oxaliplatin-resistant sub-line of the neuroblastoma cell line SK-N-AS.
Saintas, Emily; Abrahams, Liam; Ahmad, Gulshan T; Ajakaiye, Anu-Oluwa M; AlHumaidi, Abdulaziz S H A M; Ashmore-Harris, Candice; Clark, Iain; Dura, Usha K; Fixmer, Carine N; Ike-Morris, Chinedu; Mato Prado, Mireia; Mccullough, Danielle; Mishra, Shishir; Schöler, Katia M U; Timur, Husne; Williamson, Maxwell D C; Alatsatianos, Markella; Bahsoun, Basma; Blackburn, Edith; Hogwood, Catherine E; Lithgow, Pamela E; Rowe, Michelle; Yiangou, Lyto; Rothweiler, Florian; Cinatl, Jindrich; Zehner, Richard; Baines, Anthony J; Garrett, Michelle D; Gourlay, Campbell W; Griffin, Darren K; Gullick, William J; Hargreaves, Emma; Howard, Mark J; Lloyd, Daniel R; Rossman, Jeremy S; Smales, C Mark; Tsaousis, Anastasios D; von der Haar, Tobias; Wass, Mark N; Michaelis, Martin.
Afiliación
  • Saintas E; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Abrahams L; Industrial Biotechnology Centre, University of Kent, Canterbury, United Kingdom.
  • Ahmad GT; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Ajakaiye AM; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • AlHumaidi AS; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Ashmore-Harris C; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Clark I; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Dura UK; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Fixmer CN; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Ike-Morris C; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Mato Prado M; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Mccullough D; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Mishra S; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Schöler KM; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Timur H; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Williamson MD; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Alatsatianos M; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Bahsoun B; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Blackburn E; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Hogwood CE; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Lithgow PE; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Rowe M; Industrial Biotechnology Centre, University of Kent, Canterbury, United Kingdom.
  • Yiangou L; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Rothweiler F; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Cinatl J; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Zehner R; Industrial Biotechnology Centre, University of Kent, Canterbury, United Kingdom.
  • Baines AJ; Institut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
  • Garrett MD; Institut für Medizinische Virologie, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
  • Gourlay CW; Institut für Rechtsmedizin, Klinikum der Goethe-Universität, Frankfurt am Main, Germany.
  • Griffin DK; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Gullick WJ; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Hargreaves E; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Howard MJ; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Lloyd DR; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Rossman JS; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Smales CM; Industrial Biotechnology Centre, University of Kent, Canterbury, United Kingdom.
  • Tsaousis AD; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • von der Haar T; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Wass MN; School of Biosciences, University of Kent, Canterbury, United Kingdom.
  • Michaelis M; School of Biosciences, University of Kent, Canterbury, United Kingdom.
PLoS One ; 12(2): e0172140, 2017.
Article en En | MEDLINE | ID: mdl-28192521
The formation of acquired drug resistance is a major reason for the failure of anti-cancer therapies after initial response. Here, we introduce a novel model of acquired oxaliplatin resistance, a sub-line of the non-MYCN-amplified neuroblastoma cell line SK-N-AS that was adapted to growth in the presence of 4000 ng/mL oxaliplatin (SK-N-ASrOXALI4000). SK-N-ASrOXALI4000 cells displayed enhanced chromosomal aberrations compared to SK-N-AS, as indicated by 24-chromosome fluorescence in situ hybridisation. Moreover, SK-N-ASrOXALI4000 cells were resistant not only to oxaliplatin but also to the two other commonly used anti-cancer platinum agents cisplatin and carboplatin. SK-N-ASrOXALI4000 cells exhibited a stable resistance phenotype that was not affected by culturing the cells for 10 weeks in the absence of oxaliplatin. Interestingly, SK-N-ASrOXALI4000 cells showed no cross resistance to gemcitabine and increased sensitivity to doxorubicin and UVC radiation, alternative treatments that like platinum drugs target DNA integrity. Notably, UVC-induced DNA damage is thought to be predominantly repaired by nucleotide excision repair and nucleotide excision repair has been described as the main oxaliplatin-induced DNA damage repair system. SK-N-ASrOXALI4000 cells were also more sensitive to lysis by influenza A virus, a candidate for oncolytic therapy, than SK-N-AS cells. In conclusion, we introduce a novel oxaliplatin resistance model. The oxaliplatin resistance mechanisms in SK-N-ASrOXALI4000 cells appear to be complex and not to directly depend on enhanced DNA repair capacity. Models of oxaliplatin resistance are of particular relevance since research on platinum drugs has so far predominantly focused on cisplatin and carboplatin.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Compuestos Organoplatinos / Daño del ADN / Resistencia a Múltiples Medicamentos / Resistencia a Antineoplásicos Tipo de estudio: Risk_factors_studies Límite: Humans Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2017 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Compuestos Organoplatinos / Daño del ADN / Resistencia a Múltiples Medicamentos / Resistencia a Antineoplásicos Tipo de estudio: Risk_factors_studies Límite: Humans Idioma: En Revista: PLoS One Asunto de la revista: CIENCIA / MEDICINA Año: 2017 Tipo del documento: Article País de afiliación: Reino Unido Pais de publicación: Estados Unidos