In:
International Journal of Cancer, Wiley, Vol. 142, No. 11 ( 2018-06), p. 2323-2334
Kurzfassung:
What's new? The majority of pancreatic ductal adenocarcinomas (PDACs) are characterized by dysfunctional KRAS activation, which leads to persistent activation of downstream tumor‐promoting pathways. The mechanisms underlying the activation of these pathways are not fully known. In this analysis of pancreatic cancer cells and PDAC patient tissues, KRAS expression was found to be inversely correlated with expression of Raf kinase inhibitory protein (RKIP). KRAS was further found to regulate RKIP via activation of the ERK signaling pathway. In mice, injection of KRAS‐silenced pancreatic cancer cells resulted in attenuated tumor growth and increased chemosensitivity. These effects were abolished by ablation of RKIP expression.
Materialart:
Online-Ressource
ISSN:
0020-7136
,
1097-0215
Sprache:
Englisch
Verlag:
Wiley
Publikationsdatum:
2018
ZDB Id:
218257-9
ZDB Id:
1474822-8