Lipidomics reveals biomarkers of the efficacy of first-line ICI therapy combined with chemotherapy in NSCLC

脂质组学揭示了非小细胞肺癌一线免疫检查点抑制剂联合化疗疗效的生物标志物

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Abstract

BACKGROUND: Immune checkpoint inhibitors (ICIs) plus chemotherapy have become the first-line standard therapy for non-oncogene addicted advanced non-small cell lung cancer (NSCLC) patients. There is a lack of reliable biomarkers to predict treatment outcomes. This study aimed to identify relevant lipids that can predict treatment outcomes in NSCLC patients receiving first-line ICIs plus chemotherapy via lipidomics. METHOD: We recruited non-oncogene addicted advanced NSCLC patients receiving first-line ICI plus chemotherapy to participate in this study. According to the progression free survival (PFS) criteria, these patients were categorized into a response (R) group (PFS ≥ 12 months) and a non-response (NR) group (PFS < 12 months). Plasma samples were collected from patients before the start of treatment for untargeted lipidomics and semi-targeted lipidomics analysis. RESULTS: A total of 49 patients were included in this study. We screened 13 differential lipids according to P < 0.05 and AUC > 0.7. Multivariate logistic regression further identified FA-18:2 (linoleic acid, LA), PE-P-34:2, and PI-40:4 as independent predictors. The triple-lipid biomarker panel demonstrated showed good predictive performance with an AUC of 0.878. We further investigated the role of LA, a pivotal lipid involved in immune regulation, in animal and cellular models and explored its potential in enhancing NSCLC immunotherapy. Our results showed that LA synergistically enhanced PD-1 inhibitor efficacy in the Lewis lung cancer mouse model, significantly suppressing tumor growth, and downregulating PD-L1 protein expression in both tumor cells and tumor tissues. CONCLUSION: We established the lipidomics-based predictive model for the efficacy of non-oncogene addicted advanced NSCLC patients treated with first-line chemotherapy plus ICI and elucidated a novel mechanism whereby LA potentiates immunotherapy by regulating the PD-L1 pathway. These findings provide dual theoretical foundations for personalized treatment strategies and the development of immunoadjuvants.

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