Abstract
Arf-deficient mouse astrocytes and human gliom brain. Restoration of p16INK4a but not p19ARF sup FRA-promoted glioma formation.Mechanistically signaling modules in PDGFR that lost capacity to or PI3K significantly diminished PDGFRA-promot esis. Furthermore, inhibition of SHP-2 by shRNAs logical inhibitors disrupted the interaction o PDGFR , suppressed downstream AKT/mTOR a impaired tumorigenesis of Ink4a/Arf-null cells, wh sion of an activated PI3K mutant rescued the ef inhibition on tumorigenicity. PDGFR and PDG pressed in clinical GBM specimens, and such co linked with activation of SHP-2/AKT/mTOR signal Together, their data suggest that in GBMs with ciency, overexpressed PDGFRA promotes tumorige the PI3K/AKT/mTOR-mediated pathway regulated tivity. These findings functionally validate the genomi
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