PrP<sup>C</sup> contributes to increased proliferation, cell-matrix adhesion and survival in schwannoma cells acting via 37/67 kDa non-integrin laminin receptor (LR/37/67 kDa) and downstream ERK1/2, PI3K/AKT and FAK signalling pathways.
Overexpression of Akt1 was more frequent than that of Akt2 in well-differentiated liposarcoma (6/7 versus 3/7 cases) and schwannoma (4/4 versus 1/4 cases), whereas Akt2 overexpression and Akt activation were more frequent than Akt1 overexpression in malignant nerve sheath (3/4 and 4/4, respectively, versus 2/4 cases) and muscular tumors (8/9 and 8/9 versus 4/9 cases).
Due to a strong and prolonged activation of platelet-derived growth factor receptor beta (PDGFRbeta), which is highly overexpressed, ERK1/2 and AKT activation was further increased in schwannoma, leading to increased proliferation.