Tumor induction by activated JNK occurs through deregulation of cellular growth.

Abstract:

:Activation of the cytoplasmic (Ras-Raf-MEK-ERK) signaling cascade was shown to be both, necessary and sufficient for transformation in vitro as well as in vivo. However, over the last years the involvement of stress-activated protein kinases (SAPKs)/Jun N-terminal kinases (JNKs), and their substrate c-Jun in the process of cellular transformation has been suggested. To dissect the mechanisms through which JNK signaling contributes to the transformation process we employed a recently generated constitutively active version of this kinase, SAPKbeta-MKK7, which behaves like a weakly transforming oncogene in vitro. Dissection of the transforming potential of oncogenic JNK demonstrates that it is sufficient for tumor induction in nude mice. In vitro studies and analysis of tumor material support the conclusion that oncogenic JNK primarily transforms through its effects on cell proliferation and tumor vascularization but does not affect cell survival.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Rennefahrt U,Illert B,Greiner A,Rapp UR,Troppmair J

doi

10.1016/j.canlet.2004.05.015

keywords:

subject

Has Abstract

pub_date

2004-11-08 00:00:00

pages

113-24

issue

1

eissn

0304-3835

issn

1872-7980

pii

S0304-3835(04)00389-1

journal_volume

215

pub_type

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