OBJECTIVE: We recently demonstrated that the formation of CLSs in vitro, which are thought to be a reconstitution of VM, is controlled by @entity1611 . @entity16797 formation also requires the extracellular matrix signals, presumably transduced by integrins. Both pathways are affected by @entity141 . Therefore, we directly tested the roles of @entity141 and integrin in @entity320 VM. METHODS: The investigation was performed by immunocytochemical, histochemical, and 3D co-culture assays. We have also used an in vivo animal model. RESULTS: The extracellular and intracellular @entity141 chelators, EGTA and @entity11008 , prevented @entity16797 formation on Matrigel, caused actin rearrangement, and completely destroyed the preformed @entity16797 . Addition of colcemid or cytochalasin D prevented the @entity16797 formation and destroyed the preformed @entity16797 network. Herein, we also show that blocking antibodies to a  b3 and a  b5 integrins disrupted the @entity16797 network. Control blocking antibody to b1 integrin had no effect. In vivo experiments indicated that @entity141 chelation dramatically reduced the signs of @entity320 grafted in @entity19 . CONCLUSIONS: Our results indicate that the formation of @entity16797 is tightly regulated by extracellular and intracellular @entity141 levels; a  b3 and a  b5 integrins are primarily responsible for @entity16797 formation, whereas b1 integrin does not participate in @entity16797 formation.

XXXX vasculogenic mimicry capillary-like structure formation depends on integrin and calcium signaling.

@entity16797 :: ('MESH:D038921', 'Disease') :: ['CLS'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity141 :: ('CHEBI:29108', 'Chemical') :: ['Ca(2+)'] @entity1611 :: ('22339(Tax:10090)', 'Gene') :: ['VEGFA'] @entity11008 :: ('MESH:C070379', 'Chemical') :: ['BAPTA-AM'] @entity320 :: ('MESH:D008545', 'Disease') :: ['melanoma', 'VM in melanoma tumors']
@entity320 :: (MESH:D008545,Disease) :: ['Melanoma']
