Regulation by retinoic acid of ICAM-1 expression on human tumor cell lines

Bouillon, Marlène; Tessier, Philippe A.; Boulianne, Robert P.; Destrempe, Renée; Audette, Marie

doi:10.1016/0925-4439(91)90091-m

Cited by 41 publications

(21 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We found that 10 neuroblastoma cell lines expressed little or no ICAM-1, a known ligand for Mac-1, by flow cytometry (data not shown), and this is in accord with other reports. 40 Therefore, Mac-1 may bind other unknown molecule(s) or may transmit signals from GPI-linked receptors given that cooperation with Mac-1 through the lectinlike site on CD11b has been reported for CD66b. 6 Indeed, Mac-1 activation through specific binding to the lectinlike domain of the COOH-terminus of CD11b is involved in the antitumor activity of the soluble ␤-glucans lentinan and schizophyllan.…”

Section: Discussionmentioning

confidence: 99%

Antidisialoganglioside/granulocyte macrophage–colony-stimulating factor fusion protein facilitates neutrophil antibody-dependent cellular cytotoxicity and depends on FcγRII (CD32) and Mac-1 (CD11b/CD18) for enhanced effector cell adhesion and azurophil granule exocytosis

Metelitsa

Gillies

Super

et al. 2002

Blood

View full text Add to dashboard Cite

Polymorphonuclear leukocytes (PMNs) mediate antibody-dependent cellular cytotoxicity (ADCC), which is increased by the addition of granulocyte-macrophage colony-stimulating factor (GM-CSF). We sought to determine whether PMN ADCC also would be increased by the addition of an antibody/GM-CSF fusion protein and whether this would be associated with the up-regulation and activation of Mac-1 (CD11b/CD18) and with azurophil granule exocytosis. ADCC against LA-N-1 human neuroblastoma cells was evaluated with 4-hour calcein acetoxymethyl ester (calcein-AM) microcytotoxicity assay, electron microscopy, and multiparameter flow cytometry. With the calcein-AM assay, LA-N-1 cell survival was 10%, 55%, and 75% when PMN ADCC was mediated by the antidisialoganglioside (anti-GD2) immunocytokine hu14. IntroductionAntibody-cytokine fusion proteins combine the targeting ability of antibodies with the immune stimulation of cytokines for cancer immunotherapy. 1 Studies in mice of antidisialoganglioside (anti-GD2)/interleukin-2 and anti-GD2/lymphotoxin-␣ fusion proteins (immunocytokines) demonstrated the eradication of hepatic metastases of neuroblastoma 2,3 and the induction of protective immunity against melanoma. 4 These and other immunocytokine strategies have been based on the stimulation of NK-cell-or T-cell-mediated responses. Polymorphonuclear leukocytes (PMNs) constitute the largest population of white blood cells, and they can mediate antibody-dependent cellular cytotoxicity (ADCC) against tumor cells. [5][6][7][8][9] In vitro studies demonstrated the strong facilitation of PMN ADCC against neuroblastoma cells by mixing granulocytemacrophage colony-stimulating factor (GM-CSF) with an anti-GD2 antibody and by a human-mouse chimeric anti-GD2/GM-CSF immunocytokine. 5,10 Fc receptors (FcR) involved in PMN ADCC may include Fc␥RII (CD32) and Fc␥RIII (CD16), which are constitutively expressed, and Fc␥RI (CD64), which is induced by interferon-␥ and G-CSF. 11,12 In addition, Fc␣RI of PMNs may be activated by constructing bispecific monoclonal antibodies (mAbs) that recognize a target cell molecule and Fc␣RI. 13 Binding of an antibody-cytokine fusion protein to FcR may be affected by the physical presence of the cytokine or by the cytokinemodulating FcR expression. 14,15 FcRs used by PMNs in ADCC with anti-GD2/GM-CSF immunocytokines have not yet been determined.␤ 2 -Integrin receptors, particularly Mac-1 (␣ m ␤ 2 , CD11b/CD18, and complement receptor type 3), have been reported to have an essential role in PMN ADCC against neuroblastoma, lymphoma, and breast cancer cell lines. 5,13,16 Mac-1 is a major PMN ␤ 2 -integrin receptor that, on activation, acquires the ability to bind multiple ligands and to mediate several adhesion-dependent processes, including phagocytosis, superoxide production, and degranulation. 17 It recently has been demonstrated that Mac-1 function is necessary for PMN spreading on antibody-coated targets and for tumor cytolysis. 13 FcR and GM-CSF receptors activate Mac-1 For personal use only. on May 12, 2018. by ...

show abstract

Section: Discussionmentioning

confidence: 99%

Antidisialoganglioside/granulocyte macrophage–colony-stimulating factor fusion protein facilitates neutrophil antibody-dependent cellular cytotoxicity and depends on FcγRII (CD32) and Mac-1 (CD11b/CD18) for enhanced effector cell adhesion and azurophil granule exocytosis

Metelitsa

Gillies

Super

et al. 2002

Blood

View full text Add to dashboard Cite

show abstract

“…In transformed cell lines, retinoids have been shown to induce ICAM-1 expression or augment its upregulation by other known inducers of ICAM-1 (26,27). However, in primary cell cultures such as epidermal keratinocytes or EC, retinoids have not been found to induce ICAM-1 in significant amounts (28,29).…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells.

Gille¹,

Paxton²,

Lawley³

et al. 1997

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Previous investigators have reported on the RA-induced increase of mICAM-1 expression in various cell types (Bouillon et al, 1991;Wang et al, 1992;Bassi et al, 1995;Babina et al, 1997), while this study demonstrates a RA-induced increase in ICAM-1 levels in C8161 and Hs294T human melanoma cell lines. Increases in ICAM-1 expression by cytokines (Jackson et al, 1992;Cao et al, 1997;Eisenthal et al, 1998) and ICAM-1 gene transfection (Lefor and Fabian, 1998) expression and the susceptibility of RA-treated cell lines to lysis by LAK cells.…”

Section: mentioning

confidence: 42%

“…The promoter region of the gene for ICAM-1 has been shown to contain a RARE (Aoudjit et al, 1994), suggesting RA has the ability to alter ICAM-1 expression (Cilenti et al, 1995). RA is known to increase ICAM-1 expression in several cell types including melanoma cells (Bouillon et al, 1991), mast cells (Babina et al, 1997) and epithelial cells (Gao and Mackenzie, 1996). In this study, we investigate the effect of RA on its ability to alter both membrane and soluble ICAM-1 expression and the immunological consequences of such treatments in vitro.…”

mentioning

confidence: 99%

The role of human melanoma cell ICAM-1 expression on lymphokine activated killer cell-mediated lysis, and the effect of retinoic acid

1999

View full text Add to dashboard Cite

Intercellular adhesion molecule (ICAM-1) exists as a membrane-associated form (mICAM-1) on the surface of tumour cells as well as a soluble form (sICAM-1). This study analyses the ability of all- trans retinoic acid (RA) to alter both sICAM and mICAM-1 expression in C8161 and Hs294T human melanoma cell lines and investigates the involvement of ICAM-1 in the interaction between tumour and lymphokine-activated killer (LAK) cells using the Cr-51 release assay. Our data showed that 4-day pretreatment of the tumour cells with 10 −7 M RA and 10 −6 M RA induced an increase in lysis of both cell lines and also increased mICAM-1 expression without having any effect on sICAM-1 levels. Addition of blocking ICAM-1 antibody (10 μg ml −1 ) to the C8161 cells at an effector:tumour cell ratio of 40:1 caused a 2.3-fold reduction in lysis of tumour cells and a 3-fold reduction in lysis of RA-treated cells. Blocking ICAM-1 antibody at optimum concentrations of 5 μg ml −1 reduced lysis 1.8-fold in control Hs294T cells and 1.3-fold in RA-treated cells. Blocking the HLA–ABC complex had no effect on lysis. The more highly metastatic C8161 cells were found to secrete 4-fold greater levels of sICAM-1 than the poorly metastatic Hs294T cells and addition of sICAM-1 to the assay failed to affect lysis of either cell line but did induce a 2-fold decrease in lysis of RA-treated C8161 cells. Collectively, these data provide further evidence for ICAM-1 involvement in the tumour/LAK cell response and indicates that the RA-induced increase in mICAM-1 levels are partly responsible for the increase in susceptibility of the tumour cells. sICAM-1 appears to be unimportant in evasion of the tumour cells from LAK cell lysis, but may play a role in evasion of RA-treated C8161 cells. © 1999 Cancer Research Campaign

show abstract

Regulation by retinoic acid of ICAM-1 expression on human tumor cell lines

Cited by 41 publications

References 30 publications

Antidisialoganglioside/granulocyte macrophage–colony-stimulating factor fusion protein facilitates neutrophil antibody-dependent cellular cytotoxicity and depends on FcγRII (CD32) and Mac-1 (CD11b/CD18) for enhanced effector cell adhesion and azurophil granule exocytosis

Antidisialoganglioside/granulocyte macrophage–colony-stimulating factor fusion protein facilitates neutrophil antibody-dependent cellular cytotoxicity and depends on FcγRII (CD32) and Mac-1 (CD11b/CD18) for enhanced effector cell adhesion and azurophil granule exocytosis

Retinoic acid inhibits the regulated expression of vascular cell adhesion molecule-1 by cultured dermal microvascular endothelial cells.

The role of human melanoma cell ICAM-1 expression on lymphokine activated killer cell-mediated lysis, and the effect of retinoic acid

Contact Info

Product

Resources

About