Determining β 2-integrin and intercellular adhesion molecule 1 binding kinetics in tumor cell adhesion to leukocytes and endothelial cells by a gas-driven micropipette assay

Changliang Fu, Chunfang Tong, Manliu Wang, Yuxin Gao, Yan Zhang, Shouqin Lü, Shile Liang, Cheng Dong, Mian Long

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Interactions between polymorphonuclear neutrophils (PMNs) and tumor cells have been reported to facilitate the adhesion and subsequent extravasation of tumor cells through the endothelium under blood flow, both of which are mediated by binding β 2-integrin to intercellular adhesion molecule 1 (ICAM-1). Here the adhesions between humanWM9metastatic melanoma cells, PMNs, and human pulmonary microvascular endothelial cells (HPMECs) were quantified by a gas-driven micropipette aspiration technique (GDMAT). Our data indicated that the cellular binding affinity of PMN-WM9 pair was 3.9-fold higher than that of the PMN-HPMEC pair. However, the effective binding affinities per molecular pair were comparable between the two cell pairs no matter whetherWM9cells or HPMECs were quiescent or cytokine-activated, indicating that the stronger adhesion betweenPMN-WM9pair is mainly attributed to the high expression of ICAM-1 on WM9 cells. These results proposed an alternative mechanism, where WM9 melanoma cells adhere first with PMNs near vessel-wall regions and then bind to endothelial cells via PMNs under blood flow. In contrast, the adhesions between human MDA-MB-231 metastatic breast carcinoma cells and PMNs showed a comparable cellular bindingaffinitytoPMN-HPMECpairbecausetheICAM-1expressions on MDA-MB-231 cells and HPMECs are similar. Furthermore, differences were observed in the intrinsic forward and reverse rates of the β 2-integrin-ICAM-1 bond between PMN-TC and PMN-EC pairs. ThisGDMATassay enables us to quantify the binding kinetics of cell adhesion molecules physiologically expressed on nucleated cells. The findings also further the understanding of leukocyte-facilitated tumor cell adhesion from the viewpoint of molecular binding kinetics.

Original languageEnglish (US)
Pages (from-to)34777-34787
Number of pages11
JournalJournal of Biological Chemistry
Volume286
Issue number40
DOIs
StatePublished - Oct 7 2011

Fingerprint

Cell adhesion
Endothelial cells
Intercellular Adhesion Molecule-1
Cell Adhesion
Integrins
Tumors
Assays
Neutrophils
Leukocytes
Endothelial Cells
Gases
Adhesion
Kinetics
Cells
Neoplasms
Blood
Lung
Cell Adhesion Molecules
Melanoma
Cytokines

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

Fu, Changliang ; Tong, Chunfang ; Wang, Manliu ; Gao, Yuxin ; Zhang, Yan ; Lü, Shouqin ; Liang, Shile ; Dong, Cheng ; Long, Mian. / Determining β 2-integrin and intercellular adhesion molecule 1 binding kinetics in tumor cell adhesion to leukocytes and endothelial cells by a gas-driven micropipette assay. In: Journal of Biological Chemistry. 2011 ; Vol. 286, No. 40. pp. 34777-34787.
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abstract = "Interactions between polymorphonuclear neutrophils (PMNs) and tumor cells have been reported to facilitate the adhesion and subsequent extravasation of tumor cells through the endothelium under blood flow, both of which are mediated by binding β 2-integrin to intercellular adhesion molecule 1 (ICAM-1). Here the adhesions between humanWM9metastatic melanoma cells, PMNs, and human pulmonary microvascular endothelial cells (HPMECs) were quantified by a gas-driven micropipette aspiration technique (GDMAT). Our data indicated that the cellular binding affinity of PMN-WM9 pair was 3.9-fold higher than that of the PMN-HPMEC pair. However, the effective binding affinities per molecular pair were comparable between the two cell pairs no matter whetherWM9cells or HPMECs were quiescent or cytokine-activated, indicating that the stronger adhesion betweenPMN-WM9pair is mainly attributed to the high expression of ICAM-1 on WM9 cells. These results proposed an alternative mechanism, where WM9 melanoma cells adhere first with PMNs near vessel-wall regions and then bind to endothelial cells via PMNs under blood flow. In contrast, the adhesions between human MDA-MB-231 metastatic breast carcinoma cells and PMNs showed a comparable cellular bindingaffinitytoPMN-HPMECpairbecausetheICAM-1expressions on MDA-MB-231 cells and HPMECs are similar. Furthermore, differences were observed in the intrinsic forward and reverse rates of the β 2-integrin-ICAM-1 bond between PMN-TC and PMN-EC pairs. ThisGDMATassay enables us to quantify the binding kinetics of cell adhesion molecules physiologically expressed on nucleated cells. The findings also further the understanding of leukocyte-facilitated tumor cell adhesion from the viewpoint of molecular binding kinetics.",
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Determining β 2-integrin and intercellular adhesion molecule 1 binding kinetics in tumor cell adhesion to leukocytes and endothelial cells by a gas-driven micropipette assay. / Fu, Changliang; Tong, Chunfang; Wang, Manliu; Gao, Yuxin; Zhang, Yan; Lü, Shouqin; Liang, Shile; Dong, Cheng; Long, Mian.

In: Journal of Biological Chemistry, Vol. 286, No. 40, 07.10.2011, p. 34777-34787.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Determining β 2-integrin and intercellular adhesion molecule 1 binding kinetics in tumor cell adhesion to leukocytes and endothelial cells by a gas-driven micropipette assay

AU - Fu, Changliang

AU - Tong, Chunfang

AU - Wang, Manliu

AU - Gao, Yuxin

AU - Zhang, Yan

AU - Lü, Shouqin

AU - Liang, Shile

AU - Dong, Cheng

AU - Long, Mian

PY - 2011/10/7

Y1 - 2011/10/7

N2 - Interactions between polymorphonuclear neutrophils (PMNs) and tumor cells have been reported to facilitate the adhesion and subsequent extravasation of tumor cells through the endothelium under blood flow, both of which are mediated by binding β 2-integrin to intercellular adhesion molecule 1 (ICAM-1). Here the adhesions between humanWM9metastatic melanoma cells, PMNs, and human pulmonary microvascular endothelial cells (HPMECs) were quantified by a gas-driven micropipette aspiration technique (GDMAT). Our data indicated that the cellular binding affinity of PMN-WM9 pair was 3.9-fold higher than that of the PMN-HPMEC pair. However, the effective binding affinities per molecular pair were comparable between the two cell pairs no matter whetherWM9cells or HPMECs were quiescent or cytokine-activated, indicating that the stronger adhesion betweenPMN-WM9pair is mainly attributed to the high expression of ICAM-1 on WM9 cells. These results proposed an alternative mechanism, where WM9 melanoma cells adhere first with PMNs near vessel-wall regions and then bind to endothelial cells via PMNs under blood flow. In contrast, the adhesions between human MDA-MB-231 metastatic breast carcinoma cells and PMNs showed a comparable cellular bindingaffinitytoPMN-HPMECpairbecausetheICAM-1expressions on MDA-MB-231 cells and HPMECs are similar. Furthermore, differences were observed in the intrinsic forward and reverse rates of the β 2-integrin-ICAM-1 bond between PMN-TC and PMN-EC pairs. ThisGDMATassay enables us to quantify the binding kinetics of cell adhesion molecules physiologically expressed on nucleated cells. The findings also further the understanding of leukocyte-facilitated tumor cell adhesion from the viewpoint of molecular binding kinetics.

AB - Interactions between polymorphonuclear neutrophils (PMNs) and tumor cells have been reported to facilitate the adhesion and subsequent extravasation of tumor cells through the endothelium under blood flow, both of which are mediated by binding β 2-integrin to intercellular adhesion molecule 1 (ICAM-1). Here the adhesions between humanWM9metastatic melanoma cells, PMNs, and human pulmonary microvascular endothelial cells (HPMECs) were quantified by a gas-driven micropipette aspiration technique (GDMAT). Our data indicated that the cellular binding affinity of PMN-WM9 pair was 3.9-fold higher than that of the PMN-HPMEC pair. However, the effective binding affinities per molecular pair were comparable between the two cell pairs no matter whetherWM9cells or HPMECs were quiescent or cytokine-activated, indicating that the stronger adhesion betweenPMN-WM9pair is mainly attributed to the high expression of ICAM-1 on WM9 cells. These results proposed an alternative mechanism, where WM9 melanoma cells adhere first with PMNs near vessel-wall regions and then bind to endothelial cells via PMNs under blood flow. In contrast, the adhesions between human MDA-MB-231 metastatic breast carcinoma cells and PMNs showed a comparable cellular bindingaffinitytoPMN-HPMECpairbecausetheICAM-1expressions on MDA-MB-231 cells and HPMECs are similar. Furthermore, differences were observed in the intrinsic forward and reverse rates of the β 2-integrin-ICAM-1 bond between PMN-TC and PMN-EC pairs. ThisGDMATassay enables us to quantify the binding kinetics of cell adhesion molecules physiologically expressed on nucleated cells. The findings also further the understanding of leukocyte-facilitated tumor cell adhesion from the viewpoint of molecular binding kinetics.

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