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Table 1 Complement protein in the GBM tumor

From: The complement system in glioblastoma multiforme

Complement proteins Niche Mechanism Proposed effect
C1q GSC Wnt activation Stimulate GSC differentiation
  Perivascular Priming SDF-1 gradient GSC migration
  Perivascular gC1qR interaction Potentiate tumor cell invasiveness, chemoattractant
  Perivascular cC1qR interaction (IL-8, MCP-1 and IL-6 secretion) GSC migration
  Microenvironment GAM-M2 induction Immunosuppression
  Invasive gC1qR (Bradykinin induction) Tumor cell invasiveness
MBL Microenvironment GAM-M2 induction Immunosuppression
C3 Microenvironment MDSC recruitment Immunosuppression
C3b Microenvironment Treg induction (ligand for CD46) Immunosuppression
  Microenvironment GAM-M2 induction Immunosuppression
C3a/C3aR Hypoxic STAT-3 activation GSC maintenance
  GSC mTOR activation GSC maintenance
  Hypoxic NOX-4 activation, (STAT-3, HIF-α) GSC maintenance
  GSC SOX-2 activation GSC maintenance
  Microenvironment Chemotaxis immune cells  
CD46 Hypoxic Jagged-1-Notch disruption GSC maintenance
  Perivascular   
C5a/C5aR Invasive nice PKCζ activation Potentiate tumor cell invasiveness
  GSC PI3K/Akt/mTOR GSC maintenance
  GSC P21 inhibition GSC maintenance
  GSC OCT-4 expression GSC maintenance
  Perivascular MMP-9, MT1-MMP activation Increase tumor cell invasiveness
  Perivascular MCP-1 secretion Increase tumor cell invasiveness
  Perivascular TGF-β GSC differentation into vascular pericytes
  Perivascular NO secretion (iNOS/eNOS induction) GSC maintenance
  Perivascular VEGF expression Vascular tube formation
  Microenvironment Chemotaxis immune cells  
  Microenvironment Treg induction (High concentration) Immunosuppression
  Microenvironment GAM-M1 activation (balanced C activation) Anti-tumor response
  Microenvironment MDSC recruitment (ROS) Immunosuppression
C5b-C9 Perivascular bFGF release GSC dedifferentiation