Mitochondrial gene APOO reprograms lipid metabolism to influence the prognosis of breast cancer

Dynamics of mitochondrial metabolism are critical to breast cancer (BC) progression, yet the precise regulatory pathways underlying these changes remain incompletely understood. This study aimed to identify mitochondria-related prognostic genes in breast cancer, construct a mitochondria-related riskmodel, and investigate the role of apolipoprotein O (APOO) in lipid metabolic reprogramming and tumor progression.

This study employed bioinformatics methods to identify highly active genes closely associated with mitochondrial metabolism, and conducted an in-depth analysis of their correlation with patient prognosis. By applying multiple machine learning algorithms, we developed a novel mitochondrial gene-related risk assessment model. Through functional gain-of-function and loss-of-function experiments in cell lines, we precisely characterized the functions of target genes. Furthermore, protein blotting techniques were utilized to investigate the underlying mechanisms.

This study revealed a potential correlation between APOO and prognosis in BC patients. Through receiver operating characteristic (ROC) curve analysis, we confirmed APOO's high diagnostic value [area under the curve (AUC) =0.906]. Further research demonstrated that APOO knockdown inhibited BC cell proliferation, anti-apoptotic capacity, and migration. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses indicated that APOO may regulate lipid metabolism reprogramming in BC. Ultimately, suppressing APOO expression preliminarily validated this correlation.

Our research demonstrates that APOO serves as a biomarker for predicting prognosis in BC patients. APOO may influence BC progression through lipid metabolic reprogramming; however, the precise molecular mechanisms require further experimental validation. These findings suggest that APOO could represent a potential biomarker and therapeutic target for BC.