First-pass extracted concept

Src/FAK signaling axis inhibition

Candidate: concept label1 source documents4 linked claims

Jump to explainers Jump to evidence Jump to sources Jump to claims

Live refresh every 5sNext refresh in 5s

Extracted Explainers

What the tool is doing

This perturbation strategy inhibits Src and FAK to alter integrin signaling and collective cancer cell movement. The abstract links it to changes in E-cadherin dynamics and cell-cell adhesion.

Source 1DOI PubMed

Resources required

The abstract supports the need for Src and FAK inhibition during in vivo and in vitro measurements, but does not specify reagents in the source abstract itself.

Source 1DOI PubMed

What problem it solves

It is presented as a possible strategy to prevent tumor cell spread by disrupting signaling that regulates E-cadherin-mediated adhesions.

Source 1DOI PubMed

What it does not solve

The abstract does not show clinical efficacy or define which metastatic stages beyond the measured movement phenotypes are affected.

Source 1DOI PubMed

Alternatives

The abstract refers broadly to several molecularly targeted agents in clinical development, but does not name alternatives.

Source 1DOI PubMed

Evidence Snippets

We show that inhibition of Src and FAK suppresses E-cadherin-dependent collective cell movement in a complex three-dimensional tumor environment

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2010Cancer ResearchDOI PubMed

1 evidence snippet 4 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1functional effectsupports2010Source 1DOI PubMed

Inhibition of Src and FAK suppresses E-cadherin-dependent collective cell movement in a complex three-dimensional tumor environment.

Quoted textsource-backed

We show that inhibition of Src and FAK suppresses E-cadherin-dependent collective cell movement in a complex three-dimensional tumor environment

Claim 2mechanistic effectsupports2010Source 1DOI PubMed

Inhibition of Src and FAK modulates cell-cell adhesion strength and endocytosis in vitro.

Quoted textsource-backed

and modulates cell-cell adhesion strength and endocytosis in vitro

Claim 3mechanistic inferencesupports2010Source 1DOI PubMed

Integrin signaling regulates E-cadherin internalization, and this is linked to regulation of collective cancer cell movement.

Quoted textsource-backed

This shows a novel role for integrin signaling in the regulation of E-cadherin internalization, which is linked to regulation of collective cancer cell movement.

Claim 4therapeutic hypothesissupports2010Source 1DOI PubMed

Inhibition of the Src/FAK signaling axis may provide a strategy to prevent tumor cell spread by deregulating E-cadherin-mediated cell-cell adhesions.

Quoted textsource-backed

shows that inhibition of the Src/FAK signaling axis may provide a strategy to prevent tumor cell spread by deregulating E-cadherin-mediated cell-cell adhesions