期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 484, 期 4, 页码 857-863出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2017.02.003
关键词
25-Hydroxycholesterol; Lung adenocarcinoma; Migration; Invasion; LXR; IL-1 beta
资金
- National Natural Science Foundation of China [81572272, 81201778, 81201471, 81171818]
- Promotive Research Fund for Excellent Young and Middle-aged Scientists of Shandong Province [BS2011SW036, BS2013YY065]
- Foundation for Outstanding Young Scientist in Shandong Province [BS2013YY058]
- Science and Technology Development Plan Project of Shandong Province [2014GSF118157]
25-hydroxycholesterol (25-HC) is enzymatically produced by cholesterol 25-hydorxylase in various organs and is involved in many processes, including lipid metabolism, inflammation and the immune response. However, the role of 25-HC in the migration and invasion of lung adenocarcinoma (ADC) cells remains largely unknown. In this study, we demonstrated that 0.1 mu M 25-HC promoted ADC cell migration and invasion without affecting cell proliferation, especially after coculture with THP1-derived macrophages. Further investigation showed that 0.1 mu M 25-HC significantly stimulated interleukin-1 beta (IL-1 beta) secretion in a coculture system and increased the expression of LXR and Snail. IL-1 beta also mimicked the effect of 25-HC. LXR knockdown notably blocked the 25-HC-induced Snail expression, migration and invasion in both the monoculture system and the coculture system, but it did not impact the effect of IL-1 beta, which suggested that IL-1 beta functioned in an LXR-independent manner. These results suggested that 25-HC promoted ADC cell migration and invasion in an LXR-dependent manner in the monoculture system but that in the coculture system, the 25-HC-induced IL-1 beta secretion enhanced the effect of 25-HC in an LXR-independent manner. (C) 2017 Elsevier Inc. All rights reserved.
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