通过与RPS3A相互作用,BTN3A3通过调节ROS/MAPK通路来抑制清细胞细胞癌的进展
Zhangyun Li1, Mengmeng Zhang1, Sihan Chen2
1School of Life Science, Jiangsu Normal University, Xuzhou, Jiangsu, China.
Cellular signalling
|October 8, 2023
概括
高水平的Butyrophilin亚系3成员A3 (BTN3A3) 与清细胞细胞癌 (ccRCC) 的更长的存活率相关. BTN3A3通过与RPS3A相互作用并通过活性氧物种 (ROS) 调节MAPK信号传递来抑制ccRCC的进展.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 免疫学 免疫学 免疫学
背景情况:
- 布蒂罗菲林亚家族3成员A3 (BTN3A3) 是一种具有瘤抑制功能的免疫球蛋白超级家族成员.
- 清细胞细胞癌 (ccRCC) 是一种显著的恶性瘤,其中预后标志物至关重要.
研究的目的:
- 研究BTN3A3在ccRCC进展中的作用.
- 确定BTN3A3的相互作用伙伴,并阐明其在ccRCC中的分子机制.
主要方法:
- 免疫沉,然后进行质谱测量以确定BTN3A3相互作用蛋白.
- 细胞增殖,迁移和入侵测定.
- 分析线粒体功能,活性氧物种 (ROS) 水平和MAPK信号通路激活.
- 通过RNA-Seq和免疫阻塞.
主要成果:
- 高BTN3A3表达与ccRCC患者的寿命延长有关.
- BTN3A3直接与RPS3A结合,这种相互作用抑制了ccRCC细胞的增殖,迁移和入侵.
- BTN3A3和RPS3A的共同表达增加了细胞氧消耗率 (OCR) 和ROS水平.
- BTN3A3负面调节MAPK通路激活,这表明它在通过ROS和MAPK信号传递的ccRCC进展中发挥了作用.
结论:
- BTN3A3通过抑制细胞增殖,迁移和入侵,在ccRCC中起到瘤抑制作用.
- 该BTN3A3/RPS3A复合体调节ccRCC的进展,可能通过调节ROS和MAPK通路.
- 作为ccRCC的预后标志物和治疗点,BTN3A3显示出希望.
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