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

Ras-dependent extrusion requires phosphorylation of ERK... Together, these data demonstrate an unanticipated requirement for non-canonical EGFR signaling in cancer cell extrusion.
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1dependencysupports2025Source 1DOIPubMed

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
Claim 2mechanismsupports2025Source 1DOIPubMed

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.
Claim 3sufficiencysupports2025Source 1DOIPubMed

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.