ub.xmlui.mirage2.page-structure.muninLogoub.xmlui.mirage2.page-structure.openResearchArchiveLogo
    • EnglishEnglish
    • norsknorsk
  • Velg spraaknorsk 
    • EnglishEnglish
    • norsknorsk
  • Administrasjon/UB
Vis innførsel 
  •   Hjem
  • Det helsevitenskapelige fakultet
  • Institutt for farmasi
  • Artikler, rapporter og annet (farmasi)
  • Vis innførsel
  •   Hjem
  • Det helsevitenskapelige fakultet
  • Institutt for farmasi
  • Artikler, rapporter og annet (farmasi)
  • Vis innførsel
JavaScript is disabled for your browser. Some features of this site may not work without it.

Metabolic reprogramming supports the invasive phenotype in malignant melanoma

Permanent lenke
https://hdl.handle.net/10037/12443
DOI
https://doi.org/10.1016/j.canlet.2015.06.006
Thumbnail
Åpne
article.pdf (298.6Kb)
Submitted manuscript version (PDF)
Dato
2015
Type
Journal article
Tidsskriftartikkel

Forfatter
Bettum, Ingrid Johanne; Gorad, Saurabh Sayajirao; Barkovskaya, Anna; Pettersen, Solveig; Moestue, Siver Andreas; Vasiliauskaite, Kotryna; Tenstad, Ellen; Øyjord, Tove Ragnhild; Risa, Øystein; Nygaard, Vigdis; Mælandsmo, Gunhild; Prasmickaite, Lina
Sammendrag
Invasiveness is a hallmark of aggressive cancer like malignant melanoma, and factors involved in acquisition or maintenance of an invasive phenotype are attractive targets for therapy. We investigated melanoma phenotype modulation induced by the metastasis-promoting microenvironmental protein S100A4, focusing on the relationship between enhanced cellular motility, dedifferentiation and metabolic changes. In poorly motile, well-differentiated Melmet 5 cells, S100A4 stimulated migration, invasion and simultaneously down-regulated differentiation genes and modulated expression of metabolism genes. Metabolic studies confirmed suppressed mitochondrial respiration and activated glycolytic flux in the S100A4 stimulated cells, indicating a metabolic switch toward aerobic glycolysis, known as the Warburg effect. Reversal of the glycolytic switch by dichloracetate induced apoptosis and reduced cell growth, particularly in the S100A4 stimulated cells. This implies that cells with stimulated invasiveness get survival benefit from the glycolytic switch and, therefore, become more vulnerable to glycolysis inhibition. In conclusion, our data indicate that transition to the invasive phenotype in melanoma involves dedifferentiation and metabolic reprogramming from mitochondrial oxidation to glycolysis, which facilitates survival of the invasive cancer cells. Therapeutic strategies targeting the metabolic reprogramming may therefore be effective against the invasive phenotype.
Beskrivelse
Published version available in Cancer Letters. 2015;366(1):71-83.
Forlag
Elsevier
Sitering
Bettum, I. J., Gorad, S. S., Barkovskaya, A., Pettersen, S., Moestue, S. A., Vasiliauskaite, K. ... Prasmickaite, L. (2015). Metabolic reprogramming supports the invasive phenotype in malignant melanoma. Cancer Letters. 366(1):71-83
Metadata
Vis full innførsel
Samlinger
  • Artikler, rapporter og annet (farmasi) [393]

Bla

Bla i hele MuninEnheter og samlingerForfatterlisteTittelDatoBla i denne samlingenForfatterlisteTittelDato
Logg inn

Statistikk

Antall visninger
UiT

Munin bygger på DSpace

UiT Norges Arktiske Universitet
Universitetsbiblioteket
uit.no/ub - munin@ub.uit.no

Tilgjengelighetserklæring