Tobacco specific carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone suppresses a newly identified anti-tumor IGFBP-3/IGFBP-3R system in lung cancer cells

被引：18

作者：

Harada, Aki ^{[1
]}

Jogie-Brahim, Sherryline ^{[1
]}

Oh, Youngman ^{[1
]}

机构：

[1] Virginia Commonwealth Univ, Med Coll Virginia, Dept Pathol, Richmond, VA 23298 USA

来源：

LUNG CANCER | 2013年 / 80卷 / 03期

关键词：

IGFBP-3; Tobacco; NNK; Lung cancer; DNA methylation; Apoptosis; FACTOR-BINDING PROTEIN-3; NF-KAPPA-B; GROWTH-FACTOR-I; PLASMA-LEVELS; IGF-I; PROMOTER HYPERMETHYLATION; COLORECTAL-CANCER; CIGARETTE-SMOKE; FACTOR (IGF)-I; TUMOR-GROWTH;

D O I：

10.1016/j.lungcan.2013.02.016

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

IGFBP-3 is a tumor suppressor whose expression is frequently suppressed in lung cancer. NNK, the most potent tobacco carcinogen, enhanced cell proliferation of BEAS-2B normal lung epithelial cells and concomitantly suppressed IGFBP-3 expression through DNA methylation. Decreased IGFBP-3 expression and elevated levels of phospho-Akt, phospho-p65-NF-kappa B, and cyclin D1 were detected in tobacco carcinogen-induced tumorigenic derivatives of BEAS-2B. Overexpression of IGFBP-3 in NNKA, one of the derivatives, suppressed NF-kappa B activity and induced apoptosis, which was hindered by knocking-down of endogenous IGFBP-3R, an IGFBP-3 specific receptor. These results suggest that NNK inhibits IGFBP-3 expression to abrogate anti-tumor actions of the IGFBP-3/IGFBP-3R system in smoking-induced lung cancer. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

引用

页码：270 / 277

页数：8

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