# LYZ Gene as a Novel Therapeutic Target and Diagnostic Biomarker in Glioblastoma: Insights from Multi-Omics Analysis and Functional Validation

**Authors:** Nuoyan Zhu, Jiahui Wang, Liangliang Cai

PMC · DOI: 10.3390/biology15010009 · Biology · 2025-12-19

## TL;DR

This study identifies the LYZ gene as a potential new treatment target and diagnostic tool for glioblastoma, a deadly brain cancer.

## Contribution

The study introduces LYZ as a novel therapeutic target and biomarker for glioblastoma through multi-omics and functional validation.

## Key findings

- LYZ is significantly upregulated in glioblastoma tissues and linked to shorter patient survival.
- Knocking down LYZ reduces cancer cell proliferation, motility, and invasion.
- LYZ is expressed in macrophages and monocytes within glioblastoma and influences the tumor microenvironment.

## Abstract

Glioblastoma (GBM) is a highly aggressive and treatment-resistant brain tumor with a poor prognosis for patients, who typically survive for around 15 months post-diagnosis. This study identifies the lysozyme (LYZ) gene as a promising new therapeutic target and diagnostic biomarker for GBM. Using multi-omics analysis across several databases (TCGA, GTEx, GEO, and CGGA), we found that LYZ is significantly upregulated in GBM tissues and associated with shorter patient survival times. Functional enrichment analysis revealed that LYZ is located on the cell surface and plays a role in immune responses, particularly involving leukocytes. Immune infiltration analysis indicated that LYZ expression is linked to specific immune cell types, suggesting its influence on the tumor microenvironment. Single-cell analysis confirmed LYZ expression in macrophages and monocytes within GBM. Cellular experiments showed that LYZ expression differs between GBM cell lines and normal glial cells, and knocking down the LYZ gene significantly reduced cell proliferation, motility, and invasion. These findings suggest that LYZ is a viable target for GBM therapy and a potential biomarker for diagnosis, warranting further research into its mechanisms and clinical applications.

Immune checkpoint blockade is one of the current treatments for glioblastoma (GBM), which is still a very aggressive and treatment-resistant tumor of the central nervous system. This study focused on the LYZ gene to find new therapeutic targets. We performed a thorough screening of differential gene expressions between GBM and normal samples using many databases (TCGA, GTEx, GEO, and CGGA). Because LYZ is significantly upregulated in GBM tissues and is associated with shorter patient survival periods, we identified it as a gene of interest. LYZ’s position on the exterior side of the plasma membrane and its participation in leukocyte-mediated immunity were identified by functional enrichment analysis, indicating a role in cell surface immune responses. Significant associations between LYZ expression and particular immune cell types were found using immune infiltration analysis, suggesting that LYZ may have an impact on the tumor microenvironment. Within GBM, single-cell research verified LYZ expression in macrophages and monocytes. LYZ was shown to express differently in GBM cell lines than in normal glial cells, according to cellular experimental verification. The LYZ gene’s functional importance in the pathophysiology of GBM was highlighted by the dramatic reduction in cell proliferation, motility, and invasion that resulted from its knockout. These results suggest that LYZ is a viable therapeutic target and possible GBM diagnostic biomarker, which calls for more research into its mechanisms of action and potential clinical use.

## Linked entities

- **Genes:** LYZ (lysozyme) [NCBI Gene 4069]
- **Diseases:** glioblastoma (MONDO:0018177)

## Full-text entities

- **Genes:** LYZ (lysozyme) [NCBI Gene 4069] {aka AMYLD5, LYZF1, LZM}
- **Diseases:** tumor (MESH:D009369), GBM (MESH:D005909)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

9 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12784846/full.md

## References

29 references — full list in the complete paper: https://tomesphere.com/paper/PMC12784846/full.md

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Source: https://tomesphere.com/paper/PMC12784846