生物
癌症研究
克拉斯
表观遗传学
人口
基因表达谱
癌变
恶性肿瘤
细胞
胰腺癌
细胞生长
SIRT6型
生物信息学
PTEN公司
P110α
激酶
PDX1型
单细胞分析
干细胞
癌细胞
胰腺
遗传筛选
癌症
电池类型
癌症干细胞
下调和上调
肿瘤发生
基诺美
转录组
基因敲除
信号
CDKN2A
细胞培养
上皮-间质转换
CD44细胞
PI3K/AKT/mTOR通路
免疫学
信号转导
细胞生物学
细胞信号
作者
Juanjuan Shi,X. Wang,Yingying Tang,Shixin Meng,Zhengyan Zhang,Ping Lu,Junyi Xu,Feier Yu,X. Wang,Zheng Wang,Yongwei Sun,Jing Xue
出处
期刊:Gut
[BMJ]
日期:2026-01-16
卷期号:: gutjnl-2025
标识
DOI:10.1136/gutjnl-2025-336460
摘要
Background Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy characterised by remarkable cellular heterogeneity, which emerges early from the interplay of oncogenic KRAS signalling and inflammatory injury. However, the transcriptional, metabolic and functional properties of these pre-malignant cell states that initiate and drive PDAC progression remain elusive. Objective This study aimed to identify and functionally characterise the critical premalignant cell states that arise from this heterogeneity, to define novel biomarkers and targets for early intervention. Design Public and in-house scRNA-seq data of pancreatic tumour models were analysed to identify key subpopulations in early cellular heterogeneity. Genetic perturbation in KrasG12D-driven models was performed to assess functional impact. Mechanistic studies used TurboID proximity proteomics, epigenetic profiling and metabolic assays. Clinical relevance was validated in human PDAC cohorts. Results We identified LY6D as a marker of a distinct, gastric-like cell state that emerges early and persists throughout tumourigenesis. The LY6D + population exhibits conserved stemness and a unique, pan-stage dependency on oxidative phosphorylation (OXPHOS). Genetic ablation of Ly6d specifically impaired the gastric lineage and delayed tumourigenesis, while its overexpression enhanced tumourigenic and metastatic potential. Mechanistically, the glycosylphosphatidylinositol (GPI)-anchored LY6D protein scaffolds a lipid raft-associated kinase network that drives FOSL1-dependent epigenetic-transcriptional reprogramming. In human PDAC, LY6D + cells harbour stemness and Epithelial-Mesenchymal Transition (EMT) signatures, and high LY6D expression is an independent prognostic marker of poor survival. Conclusion Our work defines the LY6D + gastric-like cell state as a key driver linking early pre-malignant heterogeneity to PDAC initiation and progression. LY6D represents a pan-stage therapeutic target and a candidate biomarker for early detection and therapeutic targeting.
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