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. 2020 Dec 11;12(12):3720. doi: 10.3390/cancers12123720

Table 1.

Summary of studies investigating the Perineuronal Satellitosis process within brain tumour in in vivo and in vitro models along with the molecular mechanism proposed. Bold: is a summary title which encompass different process.

Experimental Models Molecular Mechanism Proposed References
Human
Tissue sample and Animals 		(First evidence) Histological visualisation
  • -

    “Neurophagic growth” substitution of tumour cell;

 [1,2,3,4,5,6,8,9,11,13]
Human
Tissue sample		 Metabolic exchange and migration
  • -

    Upregulation of TCA cycle and transmembrane transport of small molecules;

  • -

    CDC42 signalling and up-regulation BRCA1, SPARCL1, MMP9, MMP28 and aquaporin (AQP1 and AQP4) as well as EMT processes

 [41]
Animals
(in vitro, in vivo)		 Chemotactic attraction and migration
  • -

    VEGF, SDF1alpha, CXCR7 anchorage-dependent manner;

 [46,47]
Animals
In vivo, in vitro
Patient derived GB cells		 Metabolic exchange and spared within brain parenchyma
  • -

    Glutamate released by neurons acts: (I) “enhancer”; (II) excitotoxin;

  • -

    NMDA receptor on cancer cells uptake glutamate from neurons;

 [29,51,52,53]
Human
In vivo; in vitro
Patient derived GB cells		 Neuronal activity on glioma promotion
  • -

    Increase neuronal activity by Glutamatergic synaptic;

  • -

    Secretion of NLGN3 induce GB proliferation via PI3K/mTOR;

  • -

    AMPA-receptors drive tumour proliferation;

 [66,68,69,70]