Zhao Lin, Han Haibo, Zhou Xuantong, Gong Tongyang, Zhu Yuge, Xiao Bufan, Liu Shuchang, Zhao Wei, Wu Nan
Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Thoracic Surgery II, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Clinical Laboratory, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Int J Mol Sci. 2025 May 14;26(10):4685. doi: 10.3390/ijms26104685.
Lung adenocarcinoma (LUAD) is a leading cause of cancer-related mortality, with heme metabolism playing a critical role in tumor progression and treatment resistance. This study investigates the clinical implications of heme metabolism in LUAD, focusing on its link to ferroptosis and drug sensitivity. Using multi-omics data from TCGA-LUAD, GEO databases, and a single-cell RNA-seq cohort, we identified two molecular subtypes based on heme metabolism-related genes. We further developed a prognostic panel, termed the heme metabolism risk score (HMRS), using LASSO and multivariate Cox regression analyses. The HMRS panel effectively stratified patients into high- and low-risk groups, with high-risk patients showing enhanced tumor proliferation, suppressed ferroptosis, and resistance to chemotherapy. Single-cell analysis revealed elevated heme metabolism risk in epithelial cells correlated with tumor progression. Drug sensitivity predictions were validated in platinum-based chemotherapy cohorts, confirming HMRS as a robust prognostic tool. ABCC2 was identified as a key regulator of ferroptosis and cisplatin resistance, with in vitro experiments demonstrating that ABCC2 knockdown enhanced cisplatin-induced ferroptosis. These findings highlight HMRS as a critical tool for patient stratification and ABCC2 as a promising therapeutic target to overcome cisplatin resistance.
肺腺癌(LUAD)是癌症相关死亡的主要原因,血红素代谢在肿瘤进展和治疗耐药中起关键作用。本研究调查了LUAD中血红素代谢的临床意义,重点关注其与铁死亡和药物敏感性的联系。利用来自TCGA-LUAD、GEO数据库和单细胞RNA测序队列的多组学数据,我们基于血红素代谢相关基因确定了两种分子亚型。我们进一步使用LASSO和多变量Cox回归分析开发了一个预后模型,称为血红素代谢风险评分(HMRS)。HMRS模型有效地将患者分为高风险和低风险组,高风险患者表现出肿瘤增殖增强、铁死亡受抑制和对化疗耐药。单细胞分析显示上皮细胞中血红素代谢风险升高与肿瘤进展相关。在铂类化疗队列中验证了药物敏感性预测,证实HMRS是一种可靠的预后工具。ABCC2被确定为铁死亡和顺铂耐药的关键调节因子,体外实验表明敲低ABCC2可增强顺铂诱导的铁死亡。这些发现突出了HMRS作为患者分层的关键工具,以及ABCC2作为克服顺铂耐药的有前景的治疗靶点。