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Biology subjects

Lozano, M. D.

Publications and source records attributed to Lozano, M. D..

2 recordsLinked to original sources

RNA and protein are not interchangeable in single-cell spatial multi-omics

Spatial transcriptomics is increasingly used to infer cellular phenotypes, molecular interactions, and functional tissue organization from RNA, although most of these biological processes are ultimately mediated by proteins. Here, we directly tested the interchangeability of spatial RNA and protein measurements using paired Xenium profiling of 21 matched targets across ~1.8 million cells from primary lung adenocarcinoma and metastatic castration-resistant prostate cancer. After accounting for marker- and dataset-specific protein background, we quantified concordance at multiple levels, including single-cell detection, expression magnitude, cell-type distribution, patient-level abundance, and spatial organization. Agreement at single-cell level was strongly marker-dependent. Canonical lineage markers generally showed concordant RNA and protein patterns, whereas several molecules, including in our study PD-1, PD-L1, and LAG-3, showed little concordance across modalities. Importantly, spatial organization remained substantially more discordant between modalities than overall abundance, indicating that spatial biomarkers are not directly transferable across modalities. Together, our results show that spatial RNA and protein measurements provide largely overlapping information for lineage markers and overall abundance, but can diverse for specific molecules and for higher-order spatial features, where the two layers provide complementary rather than equivalent readouts. These findings provide practical guidance on when spatial transcriptomic readouts can be interpreted as proxies for protein and when orthogonal protein validation is advisable.

cancer biology↗

FMO4 drives lung adenocarcinoma by stabilizing the MAT2A/MAT2B complex and hindering ferroptosis

Lung cancer is the leading cause of death by cancer in the world and finding new targets is a major medical need to tackle this disease. Here, upon proteomic analysis to identify common players in oncogenic EGFR- and KRAS-driven lung adenocarcinoma mouse models, we uncovered a largely unknown protein in cancer, flavin-containing monooxygenase 4 (FMO4), whose expression was increased in lung tumors compared with adjacent lung tissue. FMO4 expression was strongly increased also in lung cancer samples from patients compared with healthy lung, and its expression level was inversely correlated with overall survival. Remarkably, in vivo deletion of FMO4 greatly decreased tumor burden and increased survival in oncogenic KRAS-driven lung adenocarcinoma mice unveiling its crucial role in tumor biology. Mechanistically, we found that FMO4 loss of function promotes ferroptosis and cooperates with ferroptosis inducers in vitro and in vivo. Moreover, FMO4 facilitates the interaction between MAT2A and MAT2B, promoting the generation of cysteine from methionine, which in turn boosts the generation of glutathione, thus protecting lung adenocarcinoma against ferroptosis. In summary we identified a new target in lung adenocarcinoma with important implications in cancer biology.

cancer biology↗