Abstract
Adhesion of cancer cells to vascular endothelial cells in target organs is an initial step in cancer metastasis. Our previous studies revealed that amphoterin-induced gene and open reading frame 2 (AMIGO2) promotes the adhesion of tumor cells to liver endothelial cells, followed by the formation of liver metastasis in a mouse model. However, the precise mechanism underlying AMIGO2-promoted the adhesion of tumor cells and liver endothelial cells remains unknown. This study was conducted to explore the role of cancer cell-derived AMIGO2-containing extracellular vesicles (EVs) in the adhesion of cancer cells to human hepatic sinusoidal endothelial cells (HHSECs). Western blotting indicated that AMIGO2 was present in EVs from AMIGO2-overexpressing MKN-28 gastric cancer cells. The efficiency of EV incorporation into HHSECs was independent of the AMIGO2 content in EVs. When EV-derived AMIGO2 was internalized in HHSECs, it significantly enhanced the adhesion of HHSECs to gastric (MKN-28 and MKN-74) and colorectal cancer cells (SW480), all of which lacked AMIGO2 expression. Thus, we identified a novel mechanism by which EV-derived AMIGO2 released from AMIGO2-expressing cancer cells stimulates endothelial cell adhesion to different cancer cells for the initiate step of liver metastasis.
Highlights
Adhesion of cancer cells to vascular endothelial cells in target organs is an initial step in cancer metastasis
Our previous study showed that the expression of AMIGO2 in tumor cells that rarely metastasize to the liver enhanced the adhesion between liver endothelial cells and liver metastases
We demonstrated for the first time that AMIGO2-containing extracellular vesicles (EVs) derived from AMIGO2-expressing cancer cells were treated with liver endothelial cells, significantly enhancing their adhesion to cancer cells
Summary
Adhesion of cancer cells to vascular endothelial cells in target organs is an initial step in cancer metastasis. Our previous studies revealed that amphoterin-induced gene and open reading frame 2 (AMIGO2) promotes the adhesion of tumor cells to liver endothelial cells, followed by the formation of liver metastasis in a mouse model. We identified a novel mechanism by which EV-derived AMIGO2 released from AMIGO2expressing cancer cells stimulates endothelial cell adhesion to different cancer cells for the initiate step of liver metastasis. It has been demonstrated that the overexpression of AMIGO2 in parental QRsP-11 cells enhanced the adhesion between liver endothelial cells and tumor cells, whereas AMIGO2 knockdown in LV12 cells attenuated their attachment to endothelial cells, and liver m etastasis[5] These observations suggest a correlation between the expression of AMIGO2 in cancer cells and their adhesion to liver endothelial cells. The mechanism underlying the adhesion between endothelial and cancer cell has not yet been elucidated
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