激光捕获显微切割
癌症研究
恶性肿瘤
显微解剖
生物标志物发现
生物标志物
发育不良
食管鳞状细胞癌
医学
食管癌
生物
细胞周期
病变
免疫组织化学
病理
蛋白质组学
肿瘤科
基底细胞
生物信息学
癌
癌症
细胞
细胞周期检查点
临床意义
DNA损伤
转录组
内科学
细胞迁移
作者
Xumiao Li,Xumiao Li,Jing Yuan,Min Gao,Jibin Liu,Min Yao,YL Zhang,Mingtao Cao,Xiaolin Hu,Hui Yang,Jun Li,Chen Li,Xiaoguang Li,Xiaoguang Li,H Wang
标识
DOI:10.1002/advs.202514343
摘要
Esophageal squamous cell carcinoma (ESCC) remains a lethal malignancy lacking reliable biomarkers for precancerous lesion monitoring and intervention. In this study, formalin-fixed, paraffin-embedded archived tissue biopsies from 134 individuals across two cohorts are collected, spanning five stages of ESCC progression. Laser capture microdissection is employed to isolate the epithelial lesion (L) and the adjacent non-lesion (N) tissues. Proteomic profiling reveals a comprehensive spatio-temporal landscape of ESCC progression, encompassing 4461 proteins. Dynamic network biomarker analysis indicates moderate dysplasia (MOD) as the critical turning stage, warranting clinical attention. A seven-protein diagnostic panel (CCDC86, GBP6, PDCD6IP, C19orf53, SF3A3, GMPPB, ARPC5) with an area under the curve (AUC) of 0.956 achieves superior early detection, and the key signatures are validated by immunohistochemistry in an independent cohort. Functional validation using malignantly transformed HET-1A cells, ESCC cells, and mouse xenograft models identifies GBP6 as a novel target: DNA damage-induced progressive loss of GBP6 promotes ESCC progression by accelerating cell cycle and inducing epithelial-mesenchymal transition. Critically, PARP1 inhibition rescues GBP6 loss by suppressing TP63 and prevents ESCC progression. Overall, this study provides a systematic proteomic atlas of ESCC progression, identifies MOD as a pivotal clinical decision point, and proposes PARP1-TP63-GBP6 axis targeting as a novel intervention strategy.
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