单细胞和批量转录组学的整合揭示了CHST6作为异常性肺纤维化和肺癌中共同的致病驱动因素
Shengqiang Mao1, Jiayi Jiang2, Zhiqiang Liu3
1Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Health, State Key Laboratory of Respiratory Health and Multimorbidity, Frontiers Science Center for Disease-related Molecular Network, Sichuan Provincial Engineering Laboratory of Precision Medicine, Precision Medicine Key Laboratory of Sichuan Province, West China Hospital, West China School of Medicine, Sichuan University, Chengdu 610041, Sichuan Province, China.
APL bioengineering
|December 19, 2025
概括
异形性肺纤维化 (IPF) 和肺腺癌 (LUAD) 在脂质代谢和免疫力方面具有共同的遗传联系. 研究人员确定CHST6是驱动这两种疾病的关键基因,这表明它是潜在的治疗点.
科学领域:
- 肺部医学 肺部医学
- 在瘤学瘤学.
- 遗传学 是一个遗传学.
背景情况:
- 异常性肺纤维化 (IPF) 是一种进展性肺病,具有增加肺癌风险,特别是肺腺癌 (LUAD).
- 在IPF和LUAD并发症之间共享的遗传机制尚未得到充分理解,需要综合的多学科研究.
研究的目的:
- 调查IPF和LUAD共患病的共同遗传和分子机制.
- 为了确定两种疾病的潜在的共同致病基因和治疗点.
主要方法:
- 利用批量和单细胞转录组分析来识别共享的差异表达基因.
- 执行拷贝数变异概况和轨迹分析,以评估恶性进展.
- 采用加权基因协同表达网络分析和机器学习来构建预后模型.
主要成果:
- 确定了308个与脂质代谢和免疫-炎症过程相关的共享差异表达基因.
- 揭示了 LUAD 和 IPF 组织上皮质和巨细胞群的显著变化.
- 在IPF中发现了具有LUAD类特征的前恶性上皮细胞亚群,并确定了CHST6作为在两种条件下都被调节的顶级预后基因.
- 验证了CHST6在促进肺癌细胞增殖,迁移和入侵中的作用.
结论:
- 阐明了LUAD和IPF之间共享的分子景观.
- 建议CHST6作为LUAD和IPF联合管理的有前途的治疗标.
- 强调了多学科方法在理解复杂疾病并发症方面的重要性.
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