Ras-dependent extrusion requires phosphorylation of ERK... Together, these data demonstrate an unanticipated requirement for non-canonical EGFR signaling in cancer cell extrusion.
First-pass extracted concept
MAPK-dependent epithelial cell extrusion
Candidate: concept label1 source documents3 linked claims
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Aliases
cancer cell extrusion, ERK-dependent extrusion
Evidence Snippets
Supporting Sources
Linked Claims
EGFR activity in Ras(Q61L)-expressing cells is required for efficient extrusion, because erlotinib treatment or EGFR deletion suppresses extrusion.
Quoted textsource-backed
Unexpectedly, however, extrusion was suppressed by erlotinib, an inhibitor of epidermal growth factor receptor (EGFR), and by deletion of EGFR. EGFR expression was not required in surrounding wild-type cells but was needed by the Ras(Q61L) cells for extrusion
Oncogenic Ras(Q61L)-driven extrusion of mammary epithelial cells requires ERK phosphorylation but not AKT activation.
Quoted textsource-backed
We examined extrusion of mammary epithelial cells caused by induction of oncogenic Ras(Q61L). Ras-dependent extrusion requires phosphorylation of ERK ... but not activation of AKT kinases.
Constitutively active MEK is sufficient to drive extrusion, and EGFR inhibition still reduces extrusion in these cells.
Quoted textsource-backed
Moreover, expression of a constitutively active MEK instead of Ras was sufficient to drive extrusion, and EGFR inhibition in these cells reduced extrusion.