AI Article Synopsis
- Second-hand smoke (SHS) is linked to lung cancer and promotes tumor growth through increased angiogenesis (the formation of new blood vessels).
- Mice exposed to SHS showed larger tumors, higher capillary density, and elevated levels of VEGF and MCP-1, along with an increase in circulating endothelial progenitor cells (EPC).
- Treatment with cerivastatin or mecamylamine countered the tumor-promoting effects of SHS, indicating that these compounds can inhibit the processes stimulated by SHS in tumor development.
Article Abstract
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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| http://dx.doi.org/10.1016/s1535-6108(03)00219-8 | DOI Listing |
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