Role of tumor-suppressive genes on LPS-induced inflammatory response

利用RAW 264.7巨噬细胞样细胞，研究了肿瘤抑制因子视网膜母细胞瘤蛋白相互作用锌指1 （RIZ1）在脂多糖（LPS）诱导的炎症反应中的作用。RIZ1与p53协同增强LPS诱导的NF-kappaB激活，并在LPS的作用下增强促炎细胞因子的产生。ADP核糖基化因子- gtpase激活蛋白（ASAP1）在细胞中组成性表达，并通过LPS刺激增强表达。ASAP1的沉默增强了促炎介质的产生，以响应LPS。巨噬细胞中一系列肿瘤相关基因参与脂多糖诱导的炎症反应。

The involvement of retinoblastoma protein-interacting zinc finger 1 (RIZ1), a tumor suppressor, in lipopolysaccharide (LPS)-induced inflammatory responses was investigated by using RAW 264.7 macrophage-like cells. RIZ1 was suggested to augment LPS-induced NF-kappaB activation in collaboration with p53 and enhance the production of proinflammatory cytokines in response to LPS. An ADP ribosylation factor-GTPase activating protein (ASAP1) is constitutively expressed in the cells and the expression was augmented by LPS stimulation. Silencing of ASAP1 enhanced the production of proinflammatory mediators in response to LPS. A series of tumor-associated genes are involved in LPS-induced inflammatory response in macrophages.