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Expression of TWEAK/Fn14 in neuroblastoma: Implications in tumorigenesis

Artikel i vetenskaplig tidskrift
Författare I. Pettersen
N. Baryawno
Frida Abel
W. H. Bakkelund
S. N. Zykova
J. O. Winberg
U. Moens
A. Rasmuson
P. Kogner
J. I. Johnsen
B. Sveinbjornsson
Publicerad i International Journal of Oncology
Volym 42
Nummer/häfte 4
Sidor 1239-1248
ISSN 1019-6439
Publiceringsår 2013
Publicerad vid Institutionen för biomedicin, avdelningen för medicinsk genetik och klinisk genetik
Sidor 1239-1248
Språk en
Länkar dx.doi.org/10.3892/ijo.2013.1800
Ämnesord neuroblastoma, tumor necrosis factor-like weak inducer of apoptosis, Fn14, nuclear factor kappa B, nf-kappa-b, weak inducer, endothelial-cells, tumor-growth, interferon-gamma, small t, receptor, fn14, activation, apoptosis
Ämneskategorier Cancer och onkologi, Molekylär medicin (genetik och patologi)

Sammanfattning

Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), a member of the tumor necrosis factor (TNF) family of cytokines, acts on responsive cells via binding to a cell surface receptor called Fn14. TWEAK binding to an Fn14 receptor or constitutive Fn14 overexpression has been shown to activate nuclear factor κB signaling which is important in tumorigenesis and cancer therapy resistance. In the present study, we demonstrate that TWEAK and Fn14 are expressed in neuroblastoma cell lines and primary tumors, and both are observed at increased levels in high-stage tumors. The treatment of neuroblastoma cell lines with recombinant TWEAK in vitro causes increased survival, and this effect is partially due to the activation of NF-κB signaling. Moreover, TWEAK induces the release of matrix metalloprotease-9 (MMP-9) in neuroblastoma cells, suggesting that TWEAK may play a role in the invasive phase of neuroblastoma tumorigenesis. TWEAK-induced cell survival was significantly reduced by silencing the TWEAK and Fn14 gene functions by siRNA. Thus, the expression of TWEAK and Fn14 in neuroblastoma suggests that TWEAK functions as an important regulator of primary neuroblastoma growth, invasion and survival and that the therapeutic intervention of the TWEAK/Fn14 pathway may be an important clinical strategy in neuroblastoma therapy.

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