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| 肺腺癌转移的基因组特征与调控机制 |
| Genomic characteristics and regulatory mechanisms of lung adenocarcinoma metastasis |
| 投稿时间：2026-06-29 修订日期：2026-08-25 |
| DOI： |
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| 中文关键词: 肺腺癌 肿瘤转移 器官特异性 协同调控 转化研究 |
| 英文关键词:lung adenocarcinoma tumor metastasis organ specificity cooperative regulation translational research |
| 基金项目:肿瘤与少突胶质细胞通过LTF/Fe3+交互促胶质母细胞瘤 治疗耐药机制研究 |
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| 中文摘要: |
| 肺腺癌（lung adenocarcinoma, LUAD）是肺癌中最常见的病理亚型，其转移具有高度异质性，是导致患者预后不良的主要原因。本文就肺腺癌脑、骨、肝转移的器官特异性基因组特征及其分子机制进行综述：脑转移依赖免疫抑制微环境建立与血脑屏障（blood-brain barrier, BBB）穿透，骨转移以趋化归巢和“溶骨-生长”循环为特征，而肝转移则体现为免疫耐受与代谢适应的协同。在此基础上，重点阐述驱动基因突变、染色体不稳定性（chromosomal instability, CIN）与表观遗传在肿瘤转移中的协同调控作用，并探讨基于CIN水平的精准干预和表观遗传耐药逆转策略，为肺腺癌转移的机制阐释与临床转化提供参考。 |
| 英文摘要: |
| Lung adenocarcinoma (LUAD) is the most common pathological subtype of lung cancer. Its metastasis is highly heterogeneous and represents the leading cause of poor prognosis. This review summarizes the organ-specific genomic characteristics and molecular mechanisms of brain, bone, and liver metastasis in LUAD: brain metastasis depends on the establishment of an immunosuppressive microenvironment and the penetration of blood-brain barrier (BBB); bone metastasis is characterized by chemotactic homing and the “osteolytic-growth” vicious cycle; and liver metastasis manifests as the synergy of immune tolerance and metabolic adaptation. On this basis, we focus on elucidating the synergistic regulatory roles of driver gene mutations, chromosomal instability (CIN), and epigenetics in tumor metastasis, and discuss precision interventions based on CIN levels and epigenetic resistance reversal strategies, aiming to provide a reference for mechanistic interpretation and clinical translation of LUAD metastasis. |
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