Integrated Analysis of Lactate-Related Genes Identifies S100A4 as a Novel Marker Promoting the Migration and Invasion of Endometrial Stromal Cell in Endometriosis.

Endometriosis is a prevalent gynecological disorder worldwide that significantly impairs the quality of life of patients and imposes a substantial economic burden. The limited efficacy and adverse effects of current pharmacological and surgical treatments highlight the urgent need for alternative diagnostic biomarkers and therapeutic targets. Recent evidence indicates that metabolic reprogramming, particularly lactate metabolism, plays a crucial role in the development and progression of endometriosis. In this study, we employed differential expression analysis to identify differentially expressed genes in endometriosis patients, and used Least Absolute Shrinkage and Selection Operator (LASSO) regression and Random Forest (RF) for feature selection and model construction. Five key genes (MRPS2, YARS2, SLC3A1, CALD1, and S100A4) were validated as highly accurate diagnostic markers. Furthermore, we conducted in-depth analysis of the regulatory activity of these key lactate metabolism-related genes and their association with immune infiltration. Additionally, we constructed a lncRNA-miRNA gene regulatory network, providing insights into the molecular mechanisms and potential therapeutic strategies. Among these key lactate metabolism-related genes, S100A4 was found to be significantly upregulated in the lesions of endometriosis and plays a pivotal role in regulating cellular invasion and metabolic reprogramming in endometriosis. Silencing of S100A4 significantly inhibited the migration and invasion ability of endometrial stromal cells, whereas overexpression of S100A4 reversed this inhibitory effect. This finding further underscores the importance of S100A4 as a potential therapeutic target. In conclusion, this study highlights the potential value of lactate-related genes as diagnostic biomarkers and therapeutic targets, especially targeting the S100A4 gene in endometrial stromal cells, which may serve as an effective therapeutic strategy to inhibit the progression of endometriosis, offering new directions for future clinical diagnosis and treatment.