Objective Interactions of tumor cells with endothelial cells(ECs),for example tumor cell adhesion and migration through the EC layer,are essential components of tumor metastasis.Intracellular calcium regulation and cytoskeletal proteins in both tumor cells and ECs provide important signaling mechanisms for the growth,angiogenesis and metastasis of tumor cells.In the present study,we investigated the influence of tumor cell-EC interactions on the intracellular calcium ion concentration([Ca2+]i)and vimentin in ECs.Methods [Ca2+]i was measured by confocal microscopy in human umbilical vein endothelial cells(HUVECs)before and after the addition of PC-3M prostate carcinoma cells.The expression and structural organization of vimentin in HUVECs was analyzed by immunofluorescence assays.The effect of heparin and nifidipine on EC [Ca2+]i and vimentin were investigated.Acrylamide,a known disruptor of intermediate filaments,was used to induce the collapse of vimentin filaments,and the distribution of calcium ions in ECs was determined.Results PC-3M cells induced a rapid [Ca2+]i elevation and lead to altered vimentin distribution in ECs at the sites of tumor cell-EC contact.Tumor cell-induced [Ca2+]i elevation was significantly inhibited by heparin and nifidipine;heparin could preserve endothelial cells to pretend a more normal vimentin structure;however,nifidipine had no obvious effects on the expression and organization of vimentin.Acrylamide-induced collapse of vimentin filaments shifted the distribution of calcium ions from the cytoplasm to the nucleus and perinuclear field in ECs.But,acrylamide could not inhibit tumor cell-induced [Ca2+]i elevation.Conclusion Rapid [Ca2+]i elevation and alterations in vimentin distribution occur in ECs at the sites of tumor cell-EC contact;the structural integrity of vimentin is partly related to the intracellular calcium ion distribution and concentration.