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Updated: Oct 22, 2025

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Canstatin represses glioma growth by inhibiting formation of VM-like structures

Yuqiang Ma1, Tao Wu1, Houjie Zhou1

  • 1Neurosurgery Department, Peking University Shenzhen Hospital, 1120 Lianhua Road, Futian District, Shenzhen 518035, People's Republic of China.

Translational Neuroscience
|August 26, 2021
PubMed

Insights

Canstatin inhibits vasculogenic mimicry (VM) in glioblastoma by reducing tumor growth and VM-like structure formation. This study suggests canstatin has a protective role in glioma by targeting key signaling pathways involved in VM.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Vasculogenic mimicry (VM) is a tumor survival mechanism distinct from angiogenesis, impacting cancer prognosis.
  • Canstatin is an endogenous inhibitor of angiogenesis, but its role in VM is not well understood.

Purpose of the Study:

  • To investigate the inhibitory effect of canstatin on vasculogenic mimicry formation in human glioblastoma cell lines.
  • To elucidate the molecular mechanisms underlying canstatin's action on VM.

Main Methods:

  • Overexpression of canstatin gene in U87 and U251 glioblastoma cell lines via lentiviral transduction.
  • In vitro Matrigel tube formation assays and in vivo xenograft glioma models in nude mice.
  • Analysis of VM-like structures, VEGF, Akt phosphorylation, Survivin, HIF-1α, and MMP-2 expression.

Main Results:

  • Canstatin overexpression significantly reduced tube formation in vitro and inhibited glioma xenograft growth in vivo.
  • Canstatin suppressed VM-like structure formation and reduced VEGF expression in tumors.
  • Canstatin decreased Akt phosphorylation, Survivin expression, HIF-1α production, and MMP-2 secretion.

Conclusions:

  • Canstatin exhibits a protective role against VM-like structure formation in glioma.
  • Canstatin likely inhibits VM by targeting signaling pathways including Akt, HIF-1α, and MMP-2.
Keywords:
HIF-1αU87VEGFcanstatingliomavasculogenic mimicry

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