Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10815263 | Cellular Signalling | 2015 | 8 Pages |
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.
Keywords
p38Bcl-xLERKPI3KECMp38-mitogen-activated protein kinaseBcl-2PLLMcl-1BMSCsBSAMAPKp38 MAPKα2β1 integrinbovine serum albuminAktSurvivalT-ALLbone marrow stromal cellsphosphatidylinositol-3 kinaseB-cell lymphoma-2B-cell lymphoma-extra largeMyeloid cell leukemia 1T-cell acute lymphoblastic leukemiaExtracellular matrixMEK-1Migrationv-akt murine thymoma viral oncogenemitogen-activated protein kinasePoly-l-lysineCollagenCollagen type Iextracellular signal-regulated kinase
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Authors
Dalila Naci, Fawzi Aoudjit,