未经证实:慢性炎症是肥胖的关键特征和结肠癌(CC)的标志。肥胖相关激素瘦素和脂联素改变肿瘤炎症基因谱,但它们在CC中的具体作用尚不清楚。我们先前已经研究了瘦素和巨噬细胞特异性介质衣康酸酯对M2样巨噬细胞的影响。本研究评估了它们对CC细胞的影响。
未经证实:HT-29CC细胞(来自年轻患者,III期CC)用瘦素治疗,脂联素,衣康酸4-辛酯(OI)或衣康酸二甲酯(DI)。在四个时间点(3、6、18和24小时)分析处理后的基因表达。
未经证实:用脂联素治疗后CCL22上调(18h时[FC16.3,p<0.001])。IL-8表达在脂联素(3小时[FC68.1,p<0.001])和瘦素治疗(6小时[FC7.3,p<0.001])后增加,而OI诱导IL-8的下调(在24小时[FC-5.0,p<0.001])。CXCL10在脂联素治疗后上调(在6小时[FC3.0,p=0.025]),并在24小时被OI和DI下调,分别为(OI[FC-10.0,p<0.001];DI[FC-10.0,p<0.001])。IL-1β在脂联素治疗后上调(3小时[FC10.6,p<0.001]),并被DI下调(24小时[FC-5.0,p<0.001])。TNF-α表达在脂联素后诱导(在6小时[FC110.7,p<0.001]),瘦素(在18小时[FC5.8,p=0.027])和OI(在3小时[FC91.1,p=0.001])。PPARγ受两种OI的影响(在3小时[FC10.1,p=0.031],在24小时[FC-10.0,p=0.031])和DI(在18小时[FC-1.7,p=0.033])。
未经证实:肥胖激素直接影响HT29CC细胞中炎症基因的表达,可能促进癌症进展。衣康酸影响HT29CC细胞中的预后标志物PPARγ。瘦素,脂联素和衣康酸可能代表肥胖和CC之间的联系。
UNASSIGNED: Chronic inflammation is a key feature of obesity and a hallmark of colon cancer (CC). The obesity-related hormones leptin and adiponectin alter inflammatory gene profiles in cancer, but their specific role in CC is unclear. We have previously studied the effects of leptin and the macrophage-specific mediator itaconate on M2-like macrophages. This current study evaluates their effects on CC cells.
UNASSIGNED: HT-29 CC cells (derived from a young patient, stage III CC) were treated with either leptin, adiponectin, 4-octyl itaconate (OI) or dimethyl itaconate (DI). Gene expression after treatment was analyzed at four time points (3, 6, 18, and 24 h).
UNASSIGNED: CCL22 was upregulated after treatment with adiponectin (at 18 h [FC 16.3, p < 0.001]). IL-8 expression increased following both adiponectin (at 3 h [FC 68.1, p < 0.001]) and leptin treatments (at 6 h [FC 7.3, p < 0.001]), while OI induced downregulation of IL-8 (at 24 h [FC -5.0, p < 0.001]). CXCL10 was upregulated after adiponectin treatment (at 6 h [FC 3.0, p = 0.025]) and downregulated by both OI and DI at 24 h, respectively (OI [FC -10.0, p < 0.001]; DI [FC -10.0, p < 0.001]). IL-1β was upregulated after adiponectin treatment (at 3 h [FC 10.6, p < 0.001]) and downregulated by DI (at 24 h [FC -5.0, p < 0.001]). TNF-α expression was induced following adiponectin (at 6 h [FC 110.7, p < 0.001]), leptin (at 18 h [FC 5.8, p = 0.027]) and OI (at 3 h [FC 91.1, p = 0.001]). PPARγ was affected by both OI (at 3 h [FC 10.1, p = 0.031], at 24 h [FC -10.0, p = 0.031]) and DI (at 18 h [FC -1.7, p = 0.033]).
UNASSIGNED: Obesity hormones directly affect inflammatory gene expression in HT29 CC cells, potentially enhancing cancer progression. Itaconate affects the prognostic marker PPARγ in HT29 CC cells. Leptin, adiponectin and itaconate may represent a link between obesity and CC.