Cervical squamous cell carcinoma (CESC) is a leading cause of cancer-related deaths in women, with oxidative stress playing a pivotal role in its progression. However, the role of oxidative stress-related genes (OSRGs) in modulating the tumor microenvironment, immune response, and prognosis remains poorly understood. This study aims to identify key OSRGs influencing CESC progression and survival outcomes, with a focus on their potential as prognostic biomarkers and therapeutic targets. We analyzed TCGA CESC data from the GDC Portal, clinical data from cBioPortal, and normal tissue expression data from GTEx. Differentially expressed genes (DEGs) between CESC and normal tissues were identified using GEPIA2. Functional annotation was performed with DAVID v6.8, and Protein-Protein Interaction (PPI) networks were constructed using STRING v11.0. A prognostic model was developed using Kaplan-Meier curves, univariate, LASSO, and multivariate regression analysis. Validation was performed using the GSE63514 dataset. We identified 3,528 upregulated and 6,865 downregulated genes in CESC, including 308 upregulated and 345 downregulated OSRGs. Key upregulated genes included CDKN2A, SLPI, and LCN2, while downregulated genes included DES, GPX3, and GSTM5. Functional enrichment analysis revealed significant associations with immune, cancer-related, and metabolic pathways. A prognostic model based on OSRG expression stratified patients into high-risk and low-risk groups with distinct survival outcomes. Validation in the GSE63514 dataset confirmed the role of CXCL8, SPP1, and PDIA3 as prognostic biomarkers. This study highlights the critical role of OSRGs in shaping the tumor microenvironment and immune response in CESC. Key prognostic markers, including CXCL8, SPP1, PDIA3, DES, and ATP13A2, were associated with poor prognosis and drug resistance. The developed risk model provides a valuable tool for survival prediction and may guide personalized treatment strategies. These findings underscore the importance of oxidative stress in CESC progression and suggest potential therapeutic targets for further investigation.