Microfibrillar-associated protein 2 is a prognostic marker that correlates with the immune microenvironment in glioma

Wanzhen Xu1, Ren Geng1, Yao Zhao1

  • 1Department of Neurosurgery, First Hospital of Jilin University, Changchun, China.

Frontiers in Genetics
|October 7, 2022
PubMed

Insights

Microfibrillar-associated protein 2 (MFAP2) is elevated in gliomas and linked to poorer patient survival. This study identifies MFAP2 as a potential prognostic marker for glioma, impacting malignant phenotypes and tumor immunity.

Area of Science:

  • Oncology
  • Molecular Biology
  • Bioinformatics

Background:

  • Microfibrillar-associated protein 2 (MFAP2) is an extracellular matrix component involved in growth factor signaling and tumor progression.
  • The role and clinicopathological significance of MFAP2 in gliomas remain largely uncharacterized.

Purpose of the Study:

  • To investigate the expression, clinicopathological correlations, immune role, and prognostic value of MFAP2 in glioma.
  • To establish a predictive model for glioma prognosis based on MFAP2.

Main Methods:

  • Analysis of MFAP2 expression in TCGA and CGGA glioma datasets.
  • Western blotting for protein validation.
  • Gene Set Enrichment Analysis (GSEA) for pathway identification.
  • Tumor immune infiltration analysis using TIMER 2.0 and TISIDB.
  • Prognostic analysis via Kaplan-Meier and Cox regression, followed by nomogram construction.

Main Results:

  • MFAP2 expression is significantly upregulated in gliomas compared to normal tissues.
  • High MFAP2 expression correlates with malignant phenotypes and poorer overall survival, DSS, and PFS.
  • MFAP2 is associated with specific immune cell infiltration (Th2, macrophages) and T-cell exhaustion markers.
  • A nomogram model incorporating MFAP2 demonstrated effective glioma prognostic prediction.

Conclusions:

  • MFAP2 serves as a potential prognostic biomarker in glioma.
  • MFAP2's role in glioma progression is linked to malignant phenotypes, cancer-related pathways, and tumor immune microenvironment modulation.