肝硫酸盐促进了TRAIL诱导的瘤细胞亡
Yin Luo1, Huanmeng Hao1, Zhangjie Wang2
1Department of Oral Biology, School of Dental Medicine, University at Buffalo, the State University of New York, Buffalo, NY 14214, USA.
bioRxiv : the preprint server for biology
|August 7, 2023
概括
肝硫酸盐 (HS) 通过促进 TRAIL 来增强与TNF相关的诱导亡联体 (TRAIL) 杀伤瘤的能力.
科学领域:
- 生物化学 生化学
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- 与TNF相关的诱导亡联体 (TRAIL) 已显示出作为抗癌疗法的潜力,但其疗效受到瘤耐药性的限制.
- 瘤对TRAIL的耐药性阻碍了其临床应用,需要对其监管机制有更深入的了解.
研究的目的:
- 为了研究肝素硫酸盐 (HS) 在调节癌细胞中 TRAIL 诱导的亡中的作用.
- 阐明背后的HS-TRAIL相互作用的分子机制及其对抗瘤活性的影响.
主要方法:
- 绑定亲和度测试用于量化 TRAIL-HS 相互作用.
- 基于细胞的测试,以评估不同HS表达的癌细胞系中TRAIL诱导的亡.
- 分析TRAIL和死亡受体5 (DR5) 复合体的形成和内化.
主要成果:
- TRAIL以高亲和力与HS结合,促进了更高阶的 TRAIL 寡合物的形成.
- 细胞表面的HS显著增强了乳腺癌和髓瘤细胞中TRAIL诱导的亡.
- HS表达水平与髓瘤细胞的 TRAIL 敏感性相关,较低的 HS 与抵抗性相关.
- HS促进了涉及TRAIL和DR5的三元复合体的形成,促进了DR5的内部化.
结论:
- 肝硫酸盐 (HS) 是TRAIL诱导的亡的一个关键调节剂,作为分子促进剂.
- 基于 TRAIL 的抗癌疗法,TRAIL-HS 相互作用是一个有前途的目标.
- 了解HS的作用对于开发更有效的策略来对抗耐 TRAIL 瘤至关重要.
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