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Updated: Oct 21, 2025

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Transcriptional control of brain tumor stem cells by a carbohydrate binding protein

Ahmad Sharanek1, Audrey Burban1, Aldo Hernandez-Corchado2

  • 1Lady Davis Institute for Medical Research, Jewish General Hospital, Montréal, QC H3T 1E2, Canada; Gerald Bronfman Department of Oncology and Division of Experimental Medicine, McGill University, Montréal, QC H4A 3T2, Canada.

Cell Reports
|September 1, 2021
PubMed

Insights

Targeting galectin1 (LGALS1) inhibits brain tumor stem cells (BTSCs) and enhances glioblastoma treatment response. This discovery offers new therapeutic strategies for glioblastoma by disrupting a key oncogenic pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Stem Cell Research

Background:

  • Glioblastoma (GBM) presents significant therapeutic challenges due to brain tumor stem cells (BTSCs) and intratumoral heterogeneity.
  • BTSCs are critical drivers of glioblastoma growth, recurrence, and resistance to therapy.

Purpose of the Study:

  • To investigate the role of LGALS1, encoding galectin1, in regulating BTSCs and glioblastoma therapy resistance.
  • To elucidate the molecular mechanisms by which galectin1 influences BTSC function and glioblastoma progression.

Main Methods:

  • Genetic deletion of LGALS1 in BTSCs.
  • Pharmacological and genetic inhibition of LGALS1 signaling.
  • Analysis of gene expression profiles and signaling pathways (STAT3, OSM, HOXA5).
  • Preclinical animal models of glioblastoma treated with ionizing radiation.

Main Results:

  • LGALS1 deletion alters BTSC gene expression, downregulating mesenchymal subtype signatures.
  • Inhibition of LGALS1 impairs BTSC self-renewal, suppresses tumorigenesis, and prolongs survival in animal models.
  • LGALS1 expression is regulated by STAT3 and OSM.
  • Galectin1 forms a complex with HOXA5, reprogramming the BTSC transcriptional landscape.

Conclusions:

  • Galectin1 is a key regulator of BTSCs and glioblastoma resistance.
  • Targeting the galectin1/HOXA5 complex represents a potential therapeutic strategy for glioblastoma.
  • Disrupting this oncogenic pathway can improve treatment response and patient outcomes.
Keywords:
EGFRvIIIHOXA5OSMOTX008STAT3galectin1glioblastomaglioma stem cellsionizing radiationmesenchymal

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