Cristin-resultat-ID: 1808680
Sist endret: 15. desember 2020, 10:44
NVI-rapporteringsår: 2020
Resultat
Vitenskapelig artikkel
2020

Tyrosine kinase inhibitors and interferon‐α increase tunneling nanotube (TNT) formation and cell adhesion in chronic myeloid leukemia (CML) cell lines (

Bidragsytere:
  • Maria Omsland
  • Vibeke Andresen
  • Stein-Erik Gullaksen
  • Maria del Pilar Ayuda-Duran
  • Mihaela Lucia Popa
  • Randi Hovland
  • mfl.

Tidsskrift

The FASEB Journal
ISSN 0892-6638
e-ISSN 1530-6860
NVI-nivå 2

Om resultatet

Vitenskapelig artikkel
Publiseringsår: 2020
Publisert online: 2020
Volum: 34
Sider: 3774 - 3791

Importkilder

Scopus-ID: 2-s2.0-85078665310

Beskrivelse Beskrivelse

Tittel

Tyrosine kinase inhibitors and interferon‐α increase tunneling nanotube (TNT) formation and cell adhesion in chronic myeloid leukemia (CML) cell lines (

Sammendrag

Chronic myeloid leukemia (CML) is a stem cell disease of the bone marrow where mechanisms of inter‐leukemic communication and cell‐to‐cell interactions are proposed to be important for optimal therapy response. Tunneling nanotubes (TNTs) are novel intercellular communication structures transporting different cargos with potential implications in therapy resistance. Here, we have investigated TNTs in CML cells and following treatment with the highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and interferon‐α (IFNα). CML cells from chronic phase CML patients as well as the blast crisis phase cell lines, Kcl‐22 and K562, formed few or no TNTs. Treatment with imatinib increased TNT formation in both Kcl‐22 and K562 cells, while nilotinib or IFNα increased TNTs in Kcl‐22 cells only where the TNT increase was associated with adherence to fibronectin‐coated surfaces, altered morphology, and reduced movement involving β1integrin. Ex vivo treated cells from chronic phase CML patients showed limited changes in TNT formation similarly to bone marrow cells from healthy individuals. Interestingly, in vivo nilotinib treatment in a Kcl‐22 subcutaneous mouse model resulted in morphological changes and TNT‐like structures in the tumor‐derived Kcl‐22 cells. Our results demonstrate that CML cells express low levels of TNTs, but CML therapeutics increase TNT formation in designated cell models indicating TNT functionality in bone marrow derived malignancies and their microenvironment.

Bidragsytere

Maria Omsland

  • Tilknyttet:
    Forfatter
    ved Klinisk institutt 2 ved Universitetet i Bergen
  • Tilknyttet:
    Forfatter
    ved National Institutes of Health

Vibeke Andresen

  • Tilknyttet:
    Forfatter
    ved Medisinsk klinikk ved Helse Bergen HF - Haukeland universitetssykehus
  • Tilknyttet:
    Forfatter
    ved Klinisk institutt 2 ved Universitetet i Bergen

Stein-Erik Gullaksen

  • Tilknyttet:
    Forfatter
    ved Medisinsk klinikk ved Helse Bergen HF - Haukeland universitetssykehus
  • Tilknyttet:
    Forfatter
    ved Klinisk institutt 2 ved Universitetet i Bergen

Maria del Pilar Ayuda-Duran

  • Tilknyttet:
    Forfatter
    ved Seksjon for molekylær cellebiologi ved Oslo universitetssykehus HF

Mihaela-Lucia Popa

Bidragsyterens navn vises på dette resultatet som Mihaela Lucia Popa
  • Tilknyttet:
    Forfatter
    ved Medisinsk klinikk ved Helse Bergen HF - Haukeland universitetssykehus
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