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Conversely to the upregulation of VEGFR2 upon MET disruption, MET stimulation by HGF caused dramatic depletion of VEGFR2 protein by 24 h (Fig. 1G).
MET disruption also decreased VEGF mRNA (Fig. 2C).
MET disruption upregulates VEGFR2, which drives compensatory tumor growth.
We found that MET disruption upregulates VEGFR2, thereby augmenting compensatory proliferation.
MET disruption upregulated VEGFR2, inducing compensatory tumor growth via VEGFR2 and MEK.
VEGFR2-mediated compensatory growth limits the anti-tumor efficacy of MET disruption.
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