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<!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 1.0 Transitional//EN" "http://www.w3.org/TR/xhtml1/DTD/xhtml1-transitional.dtd">
<html xmlns="http://www.w3.org/1999/xhtml">
<head>
<meta http-equiv="Content-Type" content="text/html; charset=utf-8" />
<title>Table 1</title>
</head>

<body>
<table>
  <tr>
    <td><table border="1" cellspacing="0" cellpadding="0">
      <tr>
        <td width="136"><strong>Signalling Pathway / Mechanism</strong></td>
        <td width="682"><strong>Effects on Glioma-Propagating Cells    (GPCs)</strong></td>
        <td width="142"><strong>Related References</strong></td>
      </tr>
      <tr>
        <td rowspan="3">Notch</td>
        <td>Activation    of Notch signalling maintains the self-renewal capacity of stem and    progenitor cells.</td>
        <td>[22]</td>
      </tr>
      <tr>
        <td>Downregulation    of NOTCH1, Delta-like-1, or Jagged-1 results in radiosensitization and    consequent glioma cell apoptosis.</td>
        <td>[24]
          &nbsp;</td>
      </tr>
      <tr>
        <td>&gamma;-secretase inhibitor    (GSI) targets Notch and depletes gliomasphere formation with concomitant    reduction in stemness expression and abrogates in vivo tumorigenicity.</td>
        <td>[23]</td>
      </tr>
      <tr>
        <td rowspan="3">Sonic    Hedgehog-Gli</td>
        <td>Mutation    driven activation of the Shh signalling pathway predisposes individuals to    paediatric medulloblastoma.</td>
        <td>[33,37,39]</td>
      </tr>
      <tr>
        <td>Hedgehog-Gli    signalling confers chemo- and radioresistance properties in GPCs and    regulates their self-renewal capacities.</td>
        <td>[26,44,45]
          &nbsp;</td>
      </tr>
      <tr>
        <td>Overexpression    of Gli1 leads to GPC chemoresistance and glioma proliferation.</td>
        <td>[46]</td>
      </tr>
      <tr>
        <td rowspan="3">EGFR/PI3K/AKT</td>
        <td>EGFR    amplification with expression of the mutant constitutively active EGFRvIII    correlates with enhanced tumorigenicity and tumor cell invasiveness.</td>
        <td>[47] </td>
      </tr>
      <tr>
        <td>Intratumoral    heterogeneity with EGFR gradient contributes to GPC tumorigenic ability and    invasiveness. </td>
        <td>[48]</td>
      </tr>
      <tr>
        <td>PI3K-AKT    module hyperactivation is associated with gliomagenesis, invasion and    contributes to GPC resistant phenotype.</td>
        <td>[14] </td>
      </tr>
      <tr>
        <td rowspan="3">Wnt</td>
        <td>Dysregulated    promoter hypermethylation of Wnt antagonists such as WIF, sFRP and Dkk is    frequently observed in GBMs.</td>
        <td>[59]</td>
      </tr>
      <tr>
        <td>Transcriptional    activation of Wnt target genes maintains the ability of GPC to self-renew.</td>
        <td>[62]</td>
      </tr>
      <tr>
        <td>Specific    targeting of &beta;-catenin improves overall    survival of mice <em>in vivo</em>.</td>
        <td>[13] </td>
      </tr>
      <tr>
        <td rowspan="3">TGF-&beta;</td>
        <td>Inhibits    the proliferation of normal epithelial cells and astrocytes whilst promoting    the aberrant proliferation of tumor cells in higher grade gliomas through    erroneous expression of cell cycle inhibitors.</td>
        <td>[65]</td>
      </tr>
      <tr>
        <td>Active    secretion of TGF-&beta; by high grade glioma cells    mediates tumor propagation, invasion and metastasis.</td>
        <td>[66] </td>
      </tr>
      <tr>
        <td>Autocrine    TGF-&beta; signalling is involved in the maintenance    of GPC stemness phenotype, and mediates GPC self-renewal capability through    the induction of LIF.</td>
        <td>[66,67] </td>
      </tr>
      <tr>
        <td rowspan="2">MELK</td>
        <td>Expression    of MELK in brain tumors corresponds to increasing histological grades and its    expression correlates with worse patient prognosis.</td>
        <td>[71,72]
          &nbsp;</td>
      </tr>
      <tr>
        <td>MELK    contributes to the proliferation of tumor cells via the phosphorylation of    FoxM1 and siRNA-mediated knockdown of <em>MELK</em> mitigates the self-renewal capacity of GPCs and their stemness genes.</td>
        <td>[73] </td>
      </tr>
      <tr>
        <td rowspan="3">ECM</td>
        <td>Increased    vascularization is associated with glioma malignancy, tumor progression and    clinical patient outcome.</td>
        <td>[75] </td>
      </tr>
      <tr>
        <td>Integrin-&alpha;6    levels were elevated in GPCs and depleting integrin-&alpha;6    abrogates self-renewal and glioma formation.</td>
        <td>[84]</td>
      </tr>
      <tr>
        <td>Higher    levels of laminin-&alpha;2 were observed in higher    grade gliomas and portend enhanced GPC survival and DNA repair machinery    following ionizing radiation.</td>
        <td>[85]</td>
      </tr>
      <tr>
        <td rowspan="3">HGF/c-Met</td>
        <td>Coexpression    of c-MET and HGF function in a feed-forward autocrine signalling loop and    correlates with glioma grades.</td>
        <td>[101,108,109,111]</td>
      </tr>
      <tr>
        <td>MET    signalling is crucial mediator in the maintenance of stem cell niche in the    brain.</td>
        <td>[122]</td>
      </tr>
      <tr>
        <td>Abrogation    of MET signalling <em>in vitro</em> and <em>in vivo</em> resulted in significant reduction in GPC    clonogenicity, proliferative and invasive abilities.</td>
        <td>[98] </td>
      </tr>
      <tr>
        <td rowspan="4">Metabolism</td>
        <td>Mutations    of IDH metabolic enzyme are frequently found in lower grade astrocytomas and    oligodendrogliomas, with better patient prognosis. Abrogation of mutant IDH1    glioma cells disrupts the regulation of the glioma phenotype.</td>
        <td>[144,145,148] 
          &nbsp;</td>
      </tr>
      <tr>
        <td>Ablation    of HK2 in GBM cells inhibits aerobic glycolysis and stimulates oxidative    glucose metabolism with elevated predisposition to therapeutic targeting    whilst overexpression of HK2 stimulates <em>in vitro</em> proliferation and survival of GPCs.</td>
        <td>[129] 
          &nbsp;</td>
      </tr>
      <tr>
        <td>Tighter    mitochondrial coupling, decreased ROS production and over-reliance on    respiration confer TMZ resistance in gliomas.</td>
        <td>[155]
          &nbsp;</td>
      </tr>
      <tr>
        <td>Increased    O<sub>2</sub>-:H<sub>2</sub>O<sub>2</sub> levels in GPCs correlate to elevated resistance to    chemotherapeutics, brain tumor disease progression and worse clinical    outcome.</td>
        <td>[18]</td>
      </tr>
    </table></td>
  </tr>
  <tr>
    <td><strong>Table 1:</strong> Signalling pathways involved in the regulation of glioma-propagating cells (GPCs).</td>
  </tr>
</table> 
					
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