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• W1983164100 endingPage "2015" @default.
• W1983164100 startingPage "2008" @default.
• W1983164100 abstract "Integrin-mediated attachment to extracellular matrix (ECM) is crucial for cancer progression. Malignant T cells such as acute lymphoblastic leukemia (T-ALL) express β1 integrins, which mediate their interactions with ECM. However, the role of these interactions in T-ALL malignancy is still poorly explored. In the present study, we investigated the effect of collagen; an abundant ECM, on T-ALL survival and migration. We found that collagen through α2β1 integrin promotes the survival of T-ALL cell lines in the absence of growth factors. T-ALL cell survival by collagen is associated with reduced caspase activation and maintenance of Mcl-1 levels. Collagen activated both ERK and p38 MAPKs but only MAPK/ERK was required for collagen-induced T-ALL survival. However, we found that α2β1 integrin promoted T-ALL migration via both ERK and p38. Together these data indicate that α2β1 integrin signaling can represent an important signaling pathway in T-ALL pathogenesis and suggest that its blockade could be beneficial in T-ALL treatment." @default.
• W1983164100 created "2016-06-24" @default.
• W1983164100 creator A5058348689 @default.
• W1983164100 creator A5085251031 @default.
• W1983164100 date "2014-09-01" @default.
• W1983164100 modified "2023-09-24" @default.
• W1983164100 title "Alpha2beta1 integrin promotes T cell survival and migration through the concomitant activation of ERK/Mcl-1 and p38 MAPK pathways" @default.
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• W1983164100 doi "https://doi.org/10.1016/j.cellsig.2014.05.016" @default.
• W1983164100 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24880062" @default.
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