Based on these results, it is plausible that the differences in ABCG1 gene expression may have resulted, at least partly, from the modulatory effect of the various rs57137919 sequences on DNA-protein interactions in the promoter region. However, whether the phenotypic outcomes are relevant to DNAprotein interactions is yet to be verified. Therefore, it will be beneficial to conduct additional MJ 15 studies to substantiate the regulatory factors and mechanisms that might be involved. Previous in vitro studies have suggested that ABCG1 is responsible for sterol efflux from cholesterol-loaded macrophage foam cells to mature HDL. Further, Wang et al. reported that macrophages lacking ABCG1 expression impaired cholesterol efflux to HDL and significantly reduced reverse cholesterol transport in vivo. Studies in cell lines showed that ABCG1, rather than ABCA1, can specifically mediate 7- ketocholesterol and 7b-hydroxycholesterol efflux from cells to HDL. These are two oxysterols existed in oxidized LDL with the oxidation at C7-position. Within human atherosclerotic lesions, 7-ketocholesterol and 7b-hydroxycholesterol exerted cytotoxic effects in promoting macrophage apoptosis ; similar findings were reported in studies using ABCG12/2 mice. Herein, we found that the ABCG1 promoter rs57137919A was associated with a significantly downregulated ABCG1 expression and attenuated cholesterol efflux, which may have led to the accumulation of specific oxysterols in macrophages and accelerated cell apoptosis. Macrophage apoptosis plays a critical role in the development of atherosclerosis. In fatty streak lesions, which form the early stage of atherosclerosis, an increase in macrophage apoptosis is atheroprotective, while in advanced atherosclerotic lesions, an increase in macrophage apoptosis leads to necrotic core development, contributing to vulnerable plaque formation and thrombosis. Gastric cancer is one of the most frequently occurring malignancies and keeps a major cause of cancer mortality all over the world. In China, there are about 360,000 T 98475 individuals die of gastric cancer every year. Though the incidence has decreased in recent years in the West, the survival is still worse. Over the past decades, great effort has been exerted to elucidate the pathogenesis of gastric cancer. However, the complex mechanism of gastric carcinogenesis is still uncovered. Accumulating evidence indicate that long-term chronic inflammation is one of the leading causes of tumorigenesis.