# Correlation of Galectin Family Expression with Glioblastoma Progression and Survival

**Authors:** Peter Curpen, Farah Ahmady, Blaine M. H. Carnie, Grace E. C. Anderson, George Kannourakis, Amit Sharma, Adrian A. Achuthan, Rodney B. Luwor

PMC · DOI: 10.3390/ijms27010417 · International Journal of Molecular Sciences · 2025-12-31

## TL;DR

This study explores how galectin proteins are linked to glioblastoma progression and poor patient survival, suggesting they could be important for diagnosis and treatment.

## Contribution

The study identifies specific galectin family members as potential biomarkers and therapeutic targets in glioblastoma.

## Key findings

- LGALS1, LGALS3, and LGALS9 are significantly upregulated in glioblastoma and correlate with poor survival.
- Galectins are involved in extracellular matrix remodelling, immune suppression, and protein homeostasis in glioblastoma.
- Genetic and functional analysis highlights galectins as key regulators of glioblastoma pathogenesis.

## Abstract

Glioblastoma is the most aggressive primary brain malignancy, characterised by extensive intra-tumoural heterogeneity, therapy resistance, and a profoundly immunosuppressive tumour microenvironment. The galectin family, a group of β-galactoside-binding lectins, has emerged as a key regulator of tumour biology, influencing oncogenesis, immune modulation, and therapy resistance. In this study, we performed an integrative bioinformatics analysis to systematically evaluate the expression patterns, prognostic significance, genetic alterations, and functional roles of galectin family members in glioblastoma. We utilised publicly available genomic datasets and computational tools to perform our analysis, including UALCAN, GEPIA, cBioPortal, STRING, GeneMANIA, DAVID, and TIMER. We identified LGALS1, LGALS3, and LGALS9 as significantly upregulated in glioblastoma, with their overexpression correlating with adverse patient survival. Functional enrichment analysis highlighted galectin-mediated pathways involved in extracellular matrix remodelling, immune dysregulation, tumour-promoting pathways, and protein processing, suggesting their pivotal role in glioblastoma pathogenesis. We also show that transcriptional and immunological signatures suggest that galectins may regulate glioblastoma immunosuppression, extracellular matrix remodelling, and protein homeostasis. Our findings provide novel insights into the oncogenic and immunoregulatory roles of galectins in glioblastoma, establishing their potential as prognostic biomarkers and therapeutic targets.

## Linked entities

- **Genes:** LGALS1 (galectin 1) [NCBI Gene 3956], LGALS3 (galectin 3) [NCBI Gene 3958], LGALS9 (galectin 9) [NCBI Gene 3965]
- **Proteins:** galectin (galectin)
- **Diseases:** glioblastoma (MONDO:0018177)

## Full-text entities

- **Genes:** LGALS1 (galectin 1) [NCBI Gene 3956] {aka GAL1, GBP}, LGALS9 (galectin 9) [NCBI Gene 3965] {aka HUAT, LGALS9A}, LGALS3 (galectin 3) [NCBI Gene 3958] {aka CBP35, GAL3, GALBP, GALIG, L31, LGALS2}
- **Diseases:** tumour (MESH:D009369), brain malignancy (MESH:D001932), immune dysregulation (OMIM:614878), Glioblastoma (MESH:D005909)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12785821/full.md

## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12785821/full.md

## References

49 references — full list in the complete paper: https://tomesphere.com/paper/PMC12785821/full.md

---
Source: https://tomesphere.com/paper/PMC12785821