Selectins induced by interleukin-1β on the human liver endothelial cells act as ligands for sialyl Lewis X-expressing human colon cancer cell metastasis

Matsushita, Yosuke; Kitajima, Shinichi; Goto, Masamichi; Tezuka, Yoshihisa; Sagara, Mitsuhisa; Imamura, Hiroshi; Tanabe, Gen; Tanaka, Sadao; Aikou, Takashi; Satô, Eiichi

doi:10.1016/s0304-3835(98)00220-1

Cited by 20 publications

(16 citation statements)

References 12 publications

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“…Seven cell surface molecules (sialyl Lewis A, sialyl Lewis X, GM1b, GD1α, integrin α4β1, annexin A2 and A6) have been previously proposed to mediate tumour cell adhesion to liver endothelial cells262728293031. However, a major limitation in confirming the importance of those molecules is that they were not tested for their involvement in liver metastasis formation in vivo 262728293031.…”

Section: Discussionmentioning

confidence: 99%

Amigo2-upregulation in Tumour Cells Facilitates Their Attachment to Liver Endothelial Cells Resulting in Liver Metastases

Kanda

Osaki

Onuma

et al. 2017

Sci Rep

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Since liver metastasis is the main cause of death in cancer patients, we attempted to identify the driver gene involved. QRsP-11 fibrosarcoma cells were injected into the spleens of syngeneic mice to isolate tumour sub-populations that colonize the liver. Cells from liver metastatic nodules were established and subsequently injected intrasplenically for selection. After 12 cycles, the cell subline LV12 was obtained. Intravenous injection of LV12 cells produced more liver metastases than QRsP-11 cells, whereas the incidence of lung metastases was similar to that of QRsP-11 cells. LV12 cells adhered to liver-derived but not to lung-derived endothelial cells. DNA chip analysis showed that amphoterin-induced gene and open reading frame 2 (Amigo2) was overexpressed in LV12 cells. siRNA-mediated knockdown of Amigo2 expression in LV12 cells attenuated liver endothelial cell adhesion. Ex vivo imaging showed that suppression of Amigo2 in luciferase-expressing LV12 cells reduced attachment/metastasis to liver to the same level as that observed with QRsP-11 cells. Forced expression of Amigo2 in QRsP-11 cells increased liver endothelial cell adhesion and liver metastasis. Additionally, Amigo2 expression in human cancers was higher in liver metastatic lesions than in primary lesions. Thus, Amigo2 regulated tumour cell adhesion to liver endothelial cells and formation of liver metastases.

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Section: Discussionmentioning

confidence: 99%

Amigo2-upregulation in Tumour Cells Facilitates Their Attachment to Liver Endothelial Cells Resulting in Liver Metastases

Kanda

Osaki

Onuma

et al. 2017

Sci Rep

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“…sLe x is a member of the Lewis blood group structures that are found at the nonreducing termini of N-linked or O-linked glycans on glycoproteins and glycolipids. sLe x has been identified as a necessary component of selectin-ligand interaction, which mediates cell-cell interaction and migration in several systems (14,28,30,36,45). To investigate the role of sLe x in epithelial repair we examined the expression of this antigen on bronchial epithelium by immunostaining.…”

Section: Discussionmentioning

confidence: 99%

“…Sialyl Lewis x (sLe x ), a fucose-containing tetrasaccharide [NeuAc␣2-3Gal␤1-4(Fuc␣1-3)GlcNAc] belonging to this family, has been recognized as a ligand for E-selectin and therefore has an important role in lymphocyte trafficking (28,36,45). This antigen has been detected in various tumors, where it mediates binding of cancerous cells to endothelial selectins, thereby promoting tumor metastasis (14,30). sLe x is also found at the nonreducing termini of N-linked or O-linked oligosaccharides on glycoproteins as well as on glycosphingolipids.…”

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confidence: 99%

Airway epithelial wound repair: role of carbohydrate sialyl Lewis^x

Allahverdian¹,

Wojcik²,

Dorscheid³

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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Epithelial repair is a complex cellular and molecular process, the details of which are still not clearly understood. Plasma membrane glycoconjugates can modulate cell function by altering the function of protein and lipids. Sialyl Lewisx(sLex), a fucose-containing tetrasaccharide, decorates membrane-bound and secreted proteins and mediates cell-cell interaction. In the present study we investigated the role of sLexin airway epithelial repair. Using immunohistochemistry, we showed an increased expression of sLexin areas of damaged bronchial epithelium compared with intact regions. Confluent monolayers of airway epithelial cells were mechanically wounded and allowed to close. Wounded monolayers were photographed for wound closure kinetics, fixed for immunocytochemical studies, or subjected to RNA extraction. Examining the expression of different α1,3-fucosyltransferases (FucT), enzymes that mediate the final step in the synthesis of sLex, we found that FucT-IV was the common gene expressed in all cell lines and primary airway epithelial cells. We demonstrated an increased expression of sLexover time after mechanical injury. Blocking of sLexwith an inhibitory antibody completely prevented epithelial repair. Our data suggest an essential functional role for sLexin epithelial repair. Further studies are necessary to explore the exact mechanism for sLexin mediating cell-cell interaction in bronchial epithelial cells to facilitate epithelial migration and repair.

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“…10,11,18 These molecules have been identified as markers of progression in carcinomas of the gastrointestinal tract, such as colorectal carcinoma, 19 -21 and have been implicated in tumor cell adhesion to the hepatic microvascular endothelial cells during liver metastasis. 7,22,23 Recently, a splice variant of CD44 was also identified as an E-selectin ligand. 24 Adhesion to VCAM-1 can be mediated by the ␣4 integrins ␣ 4 ␤ 1 (VLA-4) and…”

mentioning

confidence: 99%

The Host Inflammatory Response Promotes Liver Metastasis by Increasing Tumor Cell Arrest and Extravasation

Auguste

Fallavollita

Wang

et al. 2007

The American Journal of Pathology

145

104

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Inflammation can play a regulatory role in cancer progression and metastasis. Previously, we have shown that metastatic tumor cells entering the liver trigger a proinflammatory response involving Kupffer cell-mediated release of tumor necrosis factor-␣ and the up-regulation of vascular endothelial cell adhesion receptors, such as E-selectin. Here, we analyzed spatio-temporal aspects of the ensuing tumor-endothelial cell interaction using human colorectal carcinoma CX-1 and murine carcinoma H-59 cells and a combination of immunohistochemistry, confocal microscopy, and threedimensional reconstruction. E-selectin expression was evident mainly on sinusoidal vessels by 6 and 10 hours, The host microenvironment plays an important role in the regulation of tumor progression at the primary site. It can also facilitate tumor dissemination by promoting neovascularization and providing growth-enhancing factors to the metastatic cells at the secondary sites of growth.

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Selectins induced by interleukin-1β on the human liver endothelial cells act as ligands for sialyl Lewis X-expressing human colon cancer cell metastasis

Cited by 20 publications

References 12 publications

Amigo2-upregulation in Tumour Cells Facilitates Their Attachment to Liver Endothelial Cells Resulting in Liver Metastases

Amigo2-upregulation in Tumour Cells Facilitates Their Attachment to Liver Endothelial Cells Resulting in Liver Metastases

Airway epithelial wound repair: role of carbohydrate sialyl Lewis^x

The Host Inflammatory Response Promotes Liver Metastasis by Increasing Tumor Cell Arrest and Extravasation

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Selectins induced by interleukin-1β on the human liver endothelial cells act as ligands for sialyl Lewis X-expressing human colon cancer cell metastasis

Cited by 20 publications

References 12 publications

Amigo2-upregulation in Tumour Cells Facilitates Their Attachment to Liver Endothelial Cells Resulting in Liver Metastases

Amigo2-upregulation in Tumour Cells Facilitates Their Attachment to Liver Endothelial Cells Resulting in Liver Metastases

Airway epithelial wound repair: role of carbohydrate sialyl Lewisx

The Host Inflammatory Response Promotes Liver Metastasis by Increasing Tumor Cell Arrest and Extravasation

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Airway epithelial wound repair: role of carbohydrate sialyl Lewis^x