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Tobacco smoke promotes lung tumorigenesis by triggering IKKbeta- and JNK1-dependent inflammation.

Abstract：

:Chronic exposure to tobacco smoke, which contains over 60 tumor-initiating carcinogens, is the major risk factor for development of lung cancer, accounting for a large portion of cancer-related deaths worldwide. It is well established that tobacco smoke is a tumor initiator, but we asked whether it also acts as a tumor promoter once malignant initiation, such as caused by K-ras activation, has taken place. Here we demonstrate that repetitive exposure to tobacco smoke promotes tumor development both in carcinogen-treated mice and in transgenic mice undergoing sporadic K-ras activation in lung epithelial cells. Tumor promotion is due to induction of inflammation that results in enhanced pneumocyte proliferation and is abrogated by IKKbeta ablation in myeloid cells or inactivation of JNK1.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Takahashi H,Ogata H,Nishigaki R,Broide DH,Karin M

doi

10.1016/j.ccr.2009.12.008

subject

Has Abstract

pub_date

2010-01-19 00:00:00

pages

89-97

issue

1

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(09)00430-9

journal_volume

17

pub_type

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