在与HBV相关的肝癌中,新陈代谢的自我养以循环脂和细胞MAPK/mTOR轴之间的反为中心
Ying Zhu1,2, Yingke Zhao1,3, Zhouyu Ning1
1Minimally invasive therapy center, Shanghai Cancer Center, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Cell communication and signaling : CCS
|May 21, 2024
概括
乙型肝炎病毒 (HBV) 破坏肝脏新陈代谢,通过改变胆酸和脂通路,导致肝细胞癌 (HCC). 这会激活MAPK/mTOR信号,重编程脂质新陈代谢以自维持的循环.
科学领域:
- 肝细胞癌 (HCC) 研究研究
- 在癌症中代谢失调
- 病毒瘤学 病毒瘤学
背景情况:
- 乙型肝炎病毒 (HBV) 是肝细胞癌 (HCC) 的关键危险因素,充当肝炎预防剂.
- 代谢病毒的代谢病毒
- 这会破坏肝脏代谢平衡.
- 目前的HCC治疗选择有限,特别是在HBV相关病例中,这突显了对新型治疗点的需求.
- 了解HBV相关HCC的独特代谢特征对于开发向疗法至关重要.
研究的目的:
- 为了确定HBV相关HCC的独特代谢概况.
- 发现新的代谢标,以阻碍癌症的进展.
- 揭示在与HBV相关的HCC中赋予生存优势的代谢途径.
主要方法:
- 多omics分析包括转录组学,蛋白组学,代谢组学和脂组学.
- 在蛋白质组和转录组两级测试队列中验证发现.
- 评估MAPK和AKT信号通路活动.
主要成果:
- 在HBV相关的HCC血清中发现了明显的代谢功能障碍,包括上调的类固醇激素生物合成,初级胆酸代谢和脂代谢.
- 发现初级胆汁酸和脂激活了MAPK/mTOR通路.
- 组织代谢和脂质组学证实了血清变化,显示了脂质组成和不和脂肪酸积累的变化.
结论:
- 乙型肝炎病毒在HCC代谢中发挥着关键作用,通过初级胆酸和脂激活独特的MAPK/mTOR信号轴.
- 过度活跃的MAPK/mTOR信号驱动HCC细胞中显著的脂质代谢重编程.
- 一个涉及初级胆汁酸,脂和MAPK/mTOR信号的自我养周期有助于HCC的进展.
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