MEL-P, a GM-CSF-producing human melanoma cell line

Ciotti, Paola; Imro, A; Scudeletti, Marco; Rainero, Maria Luisa; Defferrari, R.; Ghiorzo, Paola; Indiveri, F.; Bianchi‐Scarrǎ, Giovanna

doi:10.1097/00008390-199606000-00003

Cited by 6 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Transduction of MCA106 with the GM-CSF gene did not alter the surface phenotype, except for a minor reduction in the expression of class I MHC antigens. This is in agreement with Ciotti et al [42], who reported the reduction of MHC class I expression in a modified melanoma cell line after GM-CSF secretion had attained high levels. MHC class I molecules are known to present tumor antigens to CD8 + T-cells, which can stimulate cytolytic responses [28].…”

Section: Discussionsupporting

confidence: 93%

MCA106 fibrosarcoma cells transduced with granulocyte/macrophage colony-stimulating factor are not superior to the wild-type cells in suppressing the growth of hepatic metastases

et al. 1999

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 93%

MCA106 fibrosarcoma cells transduced with granulocyte/macrophage colony-stimulating factor are not superior to the wild-type cells in suppressing the growth of hepatic metastases

et al. 1999

View full text Add to dashboard Cite

“…In addition all three cell lines secrete molecules such as IL-8 and CXCL-1 (Figure 5). We demonstrated that cells positive for surface expression of ICAM-1 (data not shown) also secrete sICAM-1, which has been extensively published as being up regulated in many tumors [25], notably in melanoma where it has been shown to be associated with disease progression [26,27] and proposed as a prognosis marker [28,29]. Of interest, and to corroborate with our hypothesis, cell lines expressing high amounts of GM-CSF were displaying metastatic competence and invasion [30,31].…”

Section: Resultsmentioning

confidence: 99%

LFA-1 and ICAM-1 expression induced during melanoma-endothelial cell co-culture favors the transendothelial migration of melanoma cell lines in vitro

et al. 2012

View full text Add to dashboard Cite

BackgroundPatients with metastatic melanoma have a poor median rate of survival. It is therefore necessary to increase our knowledge about melanoma cell dissemination which includes extravasation, where cancer cells cross the endothelial barrier. Extravasation is well understood during travelling of white blood cells, and involves integrins such as LFA-1 (composed of two chains, CD11a and CD18) expressed by T cells, while ICAM-1 is induced during inflammation by endothelial cells. Although melanoma cell lines cross endothelial cell barriers, they do not express LFA-1. We therefore hypothesized that melanoma-endothelial cell co-culture might induce the LFA-1/ICAM ligand/receptor couple during melanoma transmigration.MethodsA transwell approach has been used as well as blocking antibodies against CD11a, CD18 and ICAM-1. Data were analyzed with an epifluorescence microscope. Fluorescence intensity was quantified with the ImageJ software.ResultsWe show here that HUVEC-conditioned medium induce cell-surface expression of LFA-1 on melanoma cell lines. Similarly melanoma-conditioned medium activates ICAM-1 expression in endothelial cells. Accordingly blocking antibodies of ICAM-1, CD11a or CD18 strongly decrease melanoma transmigration. We therefore demonstrate that melanoma cells can cross endothelial monolayers in vitro due to the induction of ICAM-1 and LFA-1 occurring during the co-culture of melanoma and endothelial cells. Our data further suggest a role of LFA-1 and ICAM-1 in the formation of melanoma cell clumps enhancing tumor cell transmigration.ConclusionMelanoma-endothelial cell co-culture induces LFA-1 and ICAM-1 expression, thereby favoring in vitro melanoma trans-migration.

show abstract

“…In contrast, a number of solid tumour types constitutively express GM‐CSF including skin, head and neck squamous cell carcinoma, gliomas and meningiomas, often in conjunction with G‐CSF 10–13. Studies in vitro and in vivo have shown that GM‐CSF expression in tumour cells, endothelial cells and keratinocytes increases their proliferation and migration12, 14–17 and in vivo expression by tumour cells contributes to increased malignancy, angiogenesis and infiltration of stroma and macrophages 18. As endogenous unregulated production of GM‐CSF by some tumour types correlates with poor prognosis, it is therefore important to study how GM‐CSF may impact on various aspects of tumour growth and development, which may shed light on potential pitfalls in its use as a therapy adjuvant.…”

mentioning

confidence: 99%

Granulocyte‐macrophage colony stimulating factor induces endothelial capillary formation through induction of membrane‐type 1 matrix metalloproteinase expression in vitro

Krubasik

Eisenach

Kunz-Schughart

et al. 2007

Intl Journal of Cancer

View full text Add to dashboard Cite

In our study, we examined the mechanism by which granulocytemacrophage colony stimulating factor (GM-CSF) regulates angiogenesis using in vitro models. GM-CSF significantly increased precapillary sprout-like formation from endothelial cell spheroids seeded in type-I collagen gels and tubule formation on coculture of endothelial cells with fibroblasts. In both cases, sprout and tubule formation was highly dependent on metalloproteinase activity. Tissue Inhibitor of metalloproteinase (TIMP) profiling in the spheroid and coculture models showed inhibition by TIMP-2 but not by TIMP-1, indicative of activity of membrane-type matrix metalloproteinases (MT-MMPs). GM-CSF induced sprout formation in spheroids was found to be potently inhibited by siRNA specific for MT1-MMP. Subsequent analysis showed that GM-CSF transiently increased MT1-MMP mRNA in endothelial cells in a MEK-dependent mechanism, which led to increased surface levels of MT1-MMP. This was accompanied by an increase in MT1-MMP-dependent degradation of DQ-collagen by lysates of GM-CSF stimulated endothelial cells. GM-CSF did not increase MT1-MMP levels in fibroblasts. The effect of GM-CSF on endothelial cell sprout formation could be mimicked by adenoviral transduction of intact spheroids with virus expressing MT1-MMP, but not by transduction of endothelial cells before spheroid formation, suggesting that upregulation of MT1-MMP must only occur in cells directly involved in tubule formation. ' 2007 Wiley-Liss, Inc.

show abstract

MEL-P, a GM-CSF-producing human melanoma cell line

Cited by 6 publications

References 0 publications

MCA106 fibrosarcoma cells transduced with granulocyte/macrophage colony-stimulating factor are not superior to the wild-type cells in suppressing the growth of hepatic metastases

MCA106 fibrosarcoma cells transduced with granulocyte/macrophage colony-stimulating factor are not superior to the wild-type cells in suppressing the growth of hepatic metastases

LFA-1 and ICAM-1 expression induced during melanoma-endothelial cell co-culture favors the transendothelial migration of melanoma cell lines in vitro

Granulocyte‐macrophage colony stimulating factor induces endothelial capillary formation through induction of membrane‐type 1 matrix metalloproteinase expression in vitro

Contact Info

Product

Resources

About