Abstract
Tetraspanins associate with many proteins and are involved in numerous activities like the crosstalk between cells and matrix, tumor progression, angiogenesis, and hematopoiesis. These multiple activities are mostly executed via exosomes (Exo) or tumor-derived Exo (TEX) and are impaired in Tspan8-knockout (ko), CD151ko and Tspan8ko/CD151ko (dbko) mice and cells. Strongly impaired tumor cell dissemination RTK with limited migration and invasion relied on distorted associations with cell adhesion molecules and missing protease recruitment and was rescued by coculture with wild type (wt) Exo. Defects in early hematopoietic progenitor maturation depended on the failed association of hematopoietic growth factor receptors with CD151 and Tspan8. Constrained angiogenesis in ko mice was due to the failure of recruiting GPCR via Tspan8 and CD151. It was rescued by wt Exo. An additive impact of Tspan8ko and CD151ko in dbko cells depended on differences in preferred associations of Tspan8 and CD151. All defects relied on reduced delivery as well as uptake of Exo and TEX by ko cells. Here we did a literature search on the underlying mechanisms.
Keywords
Tspan8 knockout, CD151 knockout, Exosomes, TEX, Metastasis, Angiogenesis, Hematopoiesis