时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
Although surgical resection, targeted therapies and immune checkpoint inhibitors have substantially improved survival in selected patient subsets, the overall therapeutic benefit remains limited.；Increasing evidence suggests that these processes are not independent but are tightly interconnected; however, the molecular basis underlying their coordination remains insufficiently understood.；Despite these advances, the regulatory molecules that coordinate glycolytic reprogramming with immune modulation in LUAD remain poorly defined, limiting the development of effective metabolism-targeted therapeutic strategies.
方法
Glycolysis-based risk stratification predicts prognosis in LUAD To evaluate the prognostic significance of glycolysis in LUAD, we performed a systematic analysis using the KEGG_GLYCOLYSIS_GLUCONEOGENESIS gene set () derived from the Molecular Signatures Database (MSigDB).；The predictive performance of this model was evaluated in both the training and testing cohorts, demonstrating robust stability and reliable prognostic discrimination (Fig.；To determine whether the glycolysis risk score independently predicts clinical outcome, we performed multivariate Cox regression analyses incorporating the risk score and clinicopathological variables in both cohorts.
核心结论
Univariate Cox regression analysis was first conducted to identify glycolysis-related genes significantly associated with overall survival.；Based on the subset of glycolysis-associated genes significantly correlated with patient survival, we subsequently constructed a glycolysis-related prognostic risk model for LUAD (Fig.；Across the entire cohort, as well as in the training and testing sets, patients in the high-risk group exhibited significantly reduced overall survival (Fig. ‖ 结论：Overall, our findings identify a DEPDC1-associated glycolysis–immune regulatory axis and support the therapeutic potential of combining DEPDC1-targeted metabolic intervention with nanoparticle photodynamic therapy for LUAD treatment.
局限
The model remained stable across diverse clinical subgroups, indicating that glycolytic phenotypes not only reflect metabolic activity but also serve as reliable and generalizable predictors of clinical prognosis.；Therefore, further investigations in more clinically relevant animal models, including orthotopic or genetically engineered LUAD models, humanized or syngeneic models with checkpoint blockade combinations, are warranted to more comprehensively evaluate anti-tumor effect and long-term immune responses.；A limitation of this study is that the relatively high concentration of 200 µM fluvastatin used in vitro may limit the direct clinical translatability of our findings.
对本项目的价值
★☆☆☆☆ 相关范围内，作为背景与横向对照收录。设计 multi-omics。
全文来源
PMC JATS 全文（正文 55,649 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Synergistic fluvastatin-nanotherapy suppresses DEPDC1-associated glycolysis and exosomal CCL2 to modulate the immune microenvironment in lung adenocarcinoma.
- 期刊与标识：J Nanobiotechnology · PMID 42958526 · DOI 10.1186/s12951-026-04829-w
A 级证据分级：A 级（同行评议人体研究）
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