From our results we conclude that TNF- α-induced activation of the MAPK/ERK signaling pathway may promote breast cancer cell migration via both upregulation of MMP9, CD26 and FAP-α and concentration of these proteases, as also MT1-MMP and MMP2, in the lipid rafts. TNF-α may serve as a potential therapeutic target in breast cancers sus ceptible to..."> From our results we conclude that TNF- α-induced activation of the MAPK/ERK signaling pathway may promote breast cancer cell migration via both upregulation of MMP9, CD26 and FAP-α and concentration of these proteases, as also MT1-MMP and MMP2, in the lipid rafts. TNF-α may serve as a potential therapeutic target in breast cancers sus ceptible to..." /> From our results we conclude that TNF- α-induced activation of the MAPK/ERK signaling pathway may promote breast cancer cell migration via both upregulation of MMP9, CD26 and FAP-α and concentration of these proteases, as also MT1-MMP and MMP2, in the lipid rafts. TNF-α may serve as a potential therapeutic target in breast cancers sus ceptible to..." />

TNF- α promotes breast cancer cell migration and enhances the concentration of membrane-associated proteases in lipid rafts

Conclusions < /h3 > < p class= " a-plus-plus " > From our results we conclude that TNF- α-induced activation of the MAPK/ERK signaling pathway may promote breast cancer cell migration via both upregulation of MMP9, CD26 and FAP-α and concentration of these proteases, as also MT1-MMP and MMP2, in the lipid rafts. TNF-α may serve as a potential therapeutic target in breast cancers sus ceptible to TNF-α stimulation. < /p > < /span >
Source: Cellular Oncology - Category: Cancer & Oncology Source Type: research