# Deciphering oxidative stress contributions in vestibular schwannoma: A bioinformatics approach to novel therapeutic pathways

**Authors:** Yubin Xue, Mingyue Wang, Hongwei Ma, Xiaosheng Tan, Xiaosheng Tan, Xiaosheng Tan, Xiaosheng Tan

PMC · DOI: 10.1371/journal.pone.0336451 · 2025-11-13

## TL;DR

This study explores how oxidative stress contributes to vestibular schwannoma using bioinformatics to identify key genes and immune responses involved in tumor progression.

## Contribution

The study identifies novel oxidative stress-related genes and immune infiltration patterns in vestibular schwannoma using transcriptomic data.

## Key findings

- Fifteen oxidative stress-related differentially expressed genes were identified in vestibular schwannoma.
- Nine hub genes were found to be involved in apoptosis and immune-related pathways.
- Immune infiltration analysis showed differences in CD8+ T cells and macrophages in VS tissues.

## Abstract

Vestibular schwannoma (VS) is a benign tumor originating from Schwann cells, and its molecular pathogenesis remains poorly understood. Increasing evidence suggests oxidative stress (OS) plays a critical role in tumor development, but its involvement in VS is largely unexplored.

We analyzed two GEO transcriptomic datasets (GSE54934 and GSE56597) to identify oxidative stress-related differentially expressed genes (OSRDEGs). Functional enrichment, protein–protein interaction (PPI) network construction, hub gene identification, and immune infiltration analyses were performed to uncover potential molecular mechanisms.

Fifteen OSRDEGs were identified, and nine hub genes (IL6, CYBB, CAV1, EGFR, SELE, IL18, CDKN2A, ADIPOQ, CDH2) were screened. Enrichment analysis indicated that these genes are mainly involved in apoptosis, reactive oxygen species regulation, and immune-related pathways. Moreover, immune infiltration analysis revealed significant differences in CD8 + T cells and macrophage populations between VS and control tissues.

Our study suggests that oxidative stress may contribute to VS progression by influencing immune responses and signaling pathways. These findings provide new insights into the molecular basis of VS and may guide future experimental and therapeutic investigations.

## Linked entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569], CYBB (cytochrome b-245 beta chain) [NCBI Gene 1536], CAV1 (caveolin 1) [NCBI Gene 857], EGFR (epidermal growth factor receptor) [NCBI Gene 1956], SELE (selectin E) [NCBI Gene 6401], IL18 (interleukin 18) [NCBI Gene 3606], CDKN2A (cyclin dependent kinase inhibitor 2A) [NCBI Gene 1029], ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370], CDH2 (cadherin 2) [NCBI Gene 1000]
- **Diseases:** vestibular schwannoma (MONDO:0001569)

## Full-text entities

- **Genes:** IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CDH2 (cadherin 2) [NCBI Gene 1000] {aka ACOGS, ADHD8, ARVD14, CD325, CDHN, CDw325}, ADIPOQ (adiponectin, C1Q and collagen domain containing) [NCBI Gene 9370] {aka ACDC, ACRP30, ADIPQTL1, ADPN, APM-1, APM1}, SELE (selectin E) [NCBI Gene 6401] {aka CD62E, ELAM, ELAM1, ESEL, LECAM2, selectin-e}, EGFR (epidermal growth factor receptor) [NCBI Gene 1956] {aka ERBB, ERBB1, ERRP, HER1, NISBD2, NNCIS}, CAV1 (caveolin 1) [NCBI Gene 857] {aka BSCL3, CGL3, LCCNS, MSTP085, PPH3, VIP21}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, CDKN2A (cyclin dependent kinase inhibitor 2A) [NCBI Gene 1029] {aka ARF, CAI2, CDK4I, CDKN2, CMM2, INK4}, IL18 (interleukin 18) [NCBI Gene 3606] {aka IGIF, IL-18, IL-1g, IL1F4}, CYBB (cytochrome b-245 beta chain) [NCBI Gene 1536] {aka AMCBX2, CGD, CGDX, GP91-1, GP91-PHOX, GP91PHOX}
- **Diseases:** VS (MESH:D009464), benign tumor (MESH:D009369)
- **Chemicals:** reactive oxygen species (MESH:D017382)

## Figures

12 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12614553/full.md

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Source: https://tomesphere.com/paper/PMC12614553