PPARδ 反对者 抑制CD47表达和细胞化
Yilei Guo1,2, Bibimaryam Khan1, Juanjuan Shi2
1Department of Oncology, The Affiliated Wujin Hospital of Jiangsu University (The Wujin Clinical College of Xuzhou Medical University), Changzhou, Jiangsu, China.
Journal of cellular biochemistry
|December 5, 2024
概括
作为PPARδ对手的GSK0660降低了CD47的表达,并增强了巨细胞化,抑制了结肠癌的生长. 将GSK0660与CD47抗体结合起来,可以提高抗瘤免疫疗法的疗效.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- CD47在许多癌症中高度表达,抑制巨细胞化并促进瘤生长.
- 对于CD47基因表达的调节机制的理解尚不完全.
- 向CD47是癌症免疫治疗的一个有希望的策略.
研究的目的:
- 研究PPARδ抗剂GSK0660对CD47表达和功能在结肠癌中的影响.
- 在结肠癌模型中评估GSK0660单独和与CD47单克隆抗体结合的治疗潜力.
主要方法:
- 用GSK0660治疗结肠癌细胞,并分析CD47基因和蛋白质表达.
- 双路西法酶记者测试用于评估CD47基因的转录活性.
- 进行了体外共同培养试验,以评估巨细胞化.
- 在体内研究中,在BALB/C小鼠中植入CT-26结肠癌细胞,并用GSK0660和/或CD47抗体治疗它们.
主要成果:
- 治疗GSK0660显著降低了CD47基因和蛋白质的表达时间和剂量依赖的方式.
- GSK0660显著降低了CD47基因的转录活性.
- GSK0660在体外增强了巨细胞化.
- 在体内,GSK0660显著抑制了瘤生长.
- 与单独治疗相比,GSK0660和CD47抗体的组合显示出优异的瘤生长抑制.
结论:
- PPARδ对手GSK0660有效降低CD47的表达,并增强抗瘤免疫力.
- GSK0660证明了作为单一疗法的治疗潜力,并与CD47抗体协同作用,用于增强结肠癌免疫治疗.
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