Overexpression of macrophage migration inhibitory factor and functionally-related genes, D-DT, CD74, CD44, CXCR2 and

Mario Presti1, Emanuela Mazzon2, Maria Sofia Basile1

  • 1Department of Biomedical and Biotechnological Sciences, Biological Tower, University of Catania, Catania I-95123, Italy.

Oncology Letters
|August 22, 2018
PubMed

Insights

Macrophage migration inhibition factor (MIF) and its associated genes are upregulated in glioblastoma multiforme (GBM). While not directly correlating with survival, MIF shows a trend towards increased survival and is elevated in patients receiving neoadjuvant treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Macrophage migration inhibition factor (MIF) is a cytokine implicated in cancer progression, including cell cycle deregulation, angiogenesis, and metastasis.
  • Glioblastoma multiforme (GBM) is an aggressive brain tumor where understanding molecular drivers is crucial for effective treatment.

Purpose of the Study:

  • To investigate the expression of MIF and its associated genes (D-DT, CD74, CD44, CXCR2, CXCR4) in GBM.
  • To explore the correlation between these genes and patient overall survival.
  • To analyze MIF expression in relation to neoadjuvant treatment in GBM patients.

Main Methods:

  • Utilized The Cancer Genome Atlas (TCGA) databank.
  • Employed the cBioPortal web-based utility for data analysis.
  • Compared gene expression in GBM samples versus lower-grade gliomas.

Main Results:

  • A significant increase in the expression of most studied genes was observed in GBM compared to lower-grade gliomas.
  • No significant correlation was found between the selected genes and overall patient survival.
  • MIF expression showed a trend towards increased overall survival and was significantly elevated in patients who received neoadjuvant treatment.

Conclusions:

  • MIF and its receptors play a role in the progression and maintenance of GBM.
  • Further research into the biological significance of MIF in GBM could lead to targeted therapeutic strategies.
  • Modulating MIF function may offer a novel approach for GBM treatment.

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