Metabolomic Data on USP5 Knockdown in Lung Adenocarcinoma Cells

DescriptionThis dataset contains the processed metabolomics data underlying the findings of the research article titled "USP5-mediated deubiquitination of CD73 drives osimertinib resistance and glycolytic activation in LUAD via the PI3K/AKT pathway". This study establishes that the deubiquitinase USP5 stabilizes CD73 protein levels, thereby driving glycolytic metabolic reprogramming and acquired osimertinib resistance in lung adenocarcinoma (LUAD).Purpose of the Data:These data were generated to investigate metabolomic alterations resulting from USP5 knockdown in LUAD cells. The analysis specifically aimed to validate that the USP5/CD73 axis activates the PI3K/AKT/mTOR signaling pathway and reprograms cellular metabolism towards enhanced glycolysis, as detailed in the main manuscript.Experimental Design:Cell Model: Human lung adenocarcinoma cell line (H1299).Groups: Control cells (1299_NC) vs. USP5-knockdown cells (1299_shu5).Data Content: The uploaded Excel file contains the relative levels or peak intensities of identified metabolites. Key metabolites of interest include intermediates of the glycolytic pathway (e.g., glucose-6-phosphate, pyruvate) and its end product, lactate.Key Findings Supported by This Data:Comparative analysis demonstrates a significant reduction in the levels of key glycolytic metabolites and lactate in USP5-knockdown cells compared to controls. This reduction provides direct metabolomic evidence that USP5 promotes a glycolytic shift in LUAD cells. The findings are consistent with the reported stabilization of CD73 and subsequent activation of the PI3K/AKT/mTOR signaling pathway in the associated article.Usage Notes:This is a processed dataset summarizing metabolite changes. For detailed experimental methods regarding cell culture, USP5 knockdown, and metabolite extraction, please refer to the Materials and Methods section of the primary research paper.Relation to Main Publication:This dataset is an integral component of the mechanistic validation in the study, linking the USP5/CD73 protein stabilization axis to its functional metabolic consequences in LUAD tumorigenesis and drug resistance.