EGFRvIII uses intrinsic and extrinsic mechanisms to reduce glioma adhesion and increase migration.

ABSTRACT: A lack of biological markers has limited our ability to identify the invasive cells responsible for glioblastoma multiforme (GBM). To become migratory and invasive, cells must downregulate matrix adhesions, which could be a physical marker of invasive potential. We engineered murine astrocytes with common GBM mutations, e.g. Ink4a (Ink) or PTEN deletion and expressing a constitutively active EGF receptor truncation (EGFRvIII), to elucidate their effect on adhesion. While loss of Ink or PTEN did not affect adhesion, counterparts expressing EGFRvIII were significantly less adhesive. EGFRvIII reduced focal adhesion size and number, and these cells - with more labile adhesions - displayed enhanced migration. Regulation appears to depend not on physical recept

SUBMITTER: Banisadr A 

PROVIDER: S-EPMC7774888 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature