Tobacco smoke promotes lung tumorigenesis by triggering IKKbeta- and JNK1-dependent inflammation (Cancer Cell, 2010, 17:89-97)

報告日期: 2010/04/27
報告時間: 15:10/16:00
報告學生: 翁子洋
講評老師: 吳昭良
附件下載:

http://basicmed.med.ncku.edu.tw/admin/up_img/990423-1.pdf

Tobacco Smoke Promotes Lung Tumorigenesis by Triggering IKKβ- and JNK1-Dependent Inflammation

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

Cancer Cell. 2010 ;17(1):89-97

 

Speaker: 翁子洋

Commentator: 吳昭良 老師 

Date: 2010/04/27 15:00-15:50

Place: Room 602

 

Abstract:

Tobacco smoke (TS) contains over than 60 tumor-initiating carcinogens, such as NNK [4-(methylnitrosamino)-1-(3-pyridyl)-butanone]. Chronic exposure to tobacco smoke is also one of main risk factors for development of lung cancer and accounts for majority of lung cancer-related deaths. In this study, authors questioned that, in addition to an initiator in tumorigenesis, whether TS may play a role in malignant tumor promotion in tumorigenesis. To evaluate this question, they established carcinogen-treated mice and K-ras transgenic mice and find that TS exposure promotes lung cancer development in both murine models. Tumor promotion is due to induction of inflammation that results in enhanced pneumocyte proliferation and is reversed by IKKβ deletion in myeloid cells or inactivation of JNK1. Taken together, these results offer new mouse models  and mechanism to better understanding tumor promotion resulted from TS and the relationship between tumorigenic activity of an environmental irritant and abnormal inflammation response.

 

Reference:

1.  Tobacco smoke promotes lung tumorigenesis by triggering IKKbeta- and JNK1-dependent inflammation. Cancer Cell. 2010 ;17(1):89-97

2.  NF-kappaB: linking inflammation and immunity to cancer development and progression. Nat Rev Immunol. 2005, (10):749-59

3.  IKKbeta links inflammation and tumorigenesis in a mouse model of colitis-associated cancer. Cell. 2004;118(3):285-9