TY - JOUR
T1 - Second hand smoke stimulates tumor angiogenesis and growth
AU - Zhu, Bo Qing
AU - Heeschen, Christopher
AU - Sievers, Richard E.
AU - Karliner, Joel S.
AU - Parmley, William W.
AU - Glantz, Stanton A.
AU - Cooke, John P.
N1 - Funding Information:
This study was supported in part by grants from the National Heart, Lung, and Blood Institute (R01HL-586380), the Tobacco Related Disease Research Program (7RT-0128), Philip Morris Inc., the German Research Council (He 3044/1-1 and He 3044/2-2), the National Cancer Institute (CA-82103), and the Foundation for Cardiac Research, University of California, San Francisco. S.A.G. is a Cahan Distinguished Professor of the Flight Attendants Medical Research Institute, and J.P.C. is an established Investigator of the American Heart Association. Stanford University owns patents on the use of nicotinergic agonists or antagonists for therapeutic uses from which J.P.C. and C.H. derive royalties. This manuscript was partly presented at the American College of Cardiology 52 nd Annual Scientific Session, March 30–April 2, 2003, Chicago, Illinois.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 2003/9/1
Y1 - 2003/9/1
N2 - Exposure to second hand smoke (SHS) is believed to cause lung cancer. Pathological angiogenesis is a requisite for tumor growth. Lewis lung cancer cells were injected subcutaneously into mice, which were then exposed to sidestream smoke (SHS) or clean room air and administered vehicle, cerivastatin, or mecamylamine. SHS significantly increased tumor size, weight, capillary density, VEGF and MCP-1 levels, and circulating endothelial progenitor cells (EPC). Cerivastatin (an inhibitor of HMG-coA reductase) or mecamylamine (an inhibitor of nicotinic acetylcholine receptors) suppressed the effect of SHS to increase tumor size and capillary density. Cerivastatin reduced MCP-1 levels, whereas mecamylamine reduced VEGF levels and EPC. These studies reveal that SHS promotes tumor angiogenesis and growth. These effects of SHS are associated with increases in plasma VEGF and MCP-1 levels, and EPC, mediated in part by isoprenylation and nicotinic acetylcholine receptors.
AB - Exposure to second hand smoke (SHS) is believed to cause lung cancer. Pathological angiogenesis is a requisite for tumor growth. Lewis lung cancer cells were injected subcutaneously into mice, which were then exposed to sidestream smoke (SHS) or clean room air and administered vehicle, cerivastatin, or mecamylamine. SHS significantly increased tumor size, weight, capillary density, VEGF and MCP-1 levels, and circulating endothelial progenitor cells (EPC). Cerivastatin (an inhibitor of HMG-coA reductase) or mecamylamine (an inhibitor of nicotinic acetylcholine receptors) suppressed the effect of SHS to increase tumor size and capillary density. Cerivastatin reduced MCP-1 levels, whereas mecamylamine reduced VEGF levels and EPC. These studies reveal that SHS promotes tumor angiogenesis and growth. These effects of SHS are associated with increases in plasma VEGF and MCP-1 levels, and EPC, mediated in part by isoprenylation and nicotinic acetylcholine receptors.
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U2 - 10.1016/S1535-6108(03)00219-8
DO - 10.1016/S1535-6108(03)00219-8
M3 - Article
C2 - 14522253
AN - SCOPUS:0141746141
SN - 1535-6108
VL - 4
SP - 191
EP - 196
JO - Cancer Cell
JF - Cancer Cell
IS - 3
ER -