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001-es BibID:BIBFORM013299
Első szerző:Juhász Tamás (biológus, orvosbiológus)
Cím:Inhibition of calcineurin by cyclosporine A exerts multiple effects on human melanoma cell lines HT168 and WM35 / Juhász Tamás, Matta Csaba, Veress Gábor, Nagy Georgina, Szíjgyártó Zsolt, Molnár Zsanett, Fodor János, Zákány Róza, Gergely Pál
Dátum:2009
ISSN:1019-6439
Megjegyzések:The immunosuppressant cyclosporine A (CsA) is a specific pharmacological inhibitor of calcineurin, the Ca2+-calmodulin activated phospho-Ser/Thr-specific protein phosphatase. Although calcineurin-inhibiting compounds are applied for local treatment of psoriasis or atopic dermatitis in dermatological practice, little is known about the functions of calcineurin in epidermis-derived malignancies. We investigated the effects of CsA on two human melanoma cell lines, the metastasis forming HT168 and WM35 established from an RGP primary lesion. CsA of 2 gammaM lowered the enzyme activity by 50% and caused elevation in both mRNA and protein expression of calcineurin. Cell proliferation was diminished, as well as the cellular morphology and the actin organization were altered in both cell lines. CsA increased cell death moderately in both cell lines and reduced the metabolic activity of HT168 cells, but not that of WM35 cells. CsA also elevated the expressions of both Bcl-2 and ERK1/2. Fibronectin guided migration of HT168 cells was stimulated under the effect of CsA, while that of WM35 cells was reduced, moreover, HT168 cells switched from the expression of ß3 to ß1 integrin, but WM35 cells continued to express ß3. Based on our results we propose a multiple, partly malignancy-dependent role of calcineurin in these melanoma cell lines.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
calcineurin
cyclosporine A
migration
actin organization
integrins
apoptosis
ERK1/2
Bcl-2
Megjelenés:International Journal Of Oncology. - 34 : 4 (2009), p. 995-1003. -
További szerzők:Matta Csaba (1980-) (molekuláris biológus, genetikus, angol szakfordító) Veress Gábor (1971-) (neurobiológus) Nagy Georgina (1980-) (orvosbiológus) Szíjgyártó Zsolt (1978-) (vegyész) Molnár Zsanett (1982-) (analitikus) Fodor János (1973-) (élettanász, biotechnológus) Zákány Róza (1963-) (anatómus-, kötőszövetbiológus) Gergely Pál (1947-) (biokémikus)
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DOI
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001-es BibID:BIBFORM023148
Első szerző:Kitoh, Yusuke
Cím:Combined GM-CSF treatment and M-CSF inhibition of tumor-associated macrophages induces dendritic cell-like signaling in vitro / Yusuke Kitoh, Masanao Saio, Naoe Gotoh, Naoki Umemura, Kenichi Nonaka, Juncheng Bai, Laura Vizkeleti, Daniel Torocsik, Margit Balazs, Roza Adany, Tsuyoshi Takami
Dátum:2011
ISSN:1019-6439
Megjegyzések:Macrophages demonstrate plasticity, and tumor-associated macrophages (TAM) can function as immunosuppressive cells in the tumor microenvironment. Therefore, in this study, we aimed to reprogram TAM in vitro with cytokine signal alteration. Granulocyte macrophage colony stimulating factor (GM-CSF) treatment alone did not lead to changes in the expression of M1 (including IL-1?, TNF? and CXCL-10) or M2 (including CD36, CD206 and CCL17) molecules by TAM in vitro, although they adopted a round morphology and were less adhesive to the culture dish. When macrophage colony stimulating factor (M-CSF) signals were suppressed by siRNA against the M-CSF receptor (M-CSFR) in conjunction with GM-CSF treatment, the signal transduction pathway of TAM was altered, and the expression of STAT1, STAT5 and STAT6, which are usually expressed by dendritic cells, was increased. However, the same treatment did not alter the TAM expression pattern of M1/M2 marker molecules. With respect to the NF-?B pathway, GM-CSF and M-CSFR siRNA combination treatment significantly induced the expression of p65, which is usually not expressed by TAM, while p50 and p105 expression by TAM was not affected by the treatment. These findings indicate that our model could not redirect TAM to a monocyte-derived dendritic cell-like phenotype based on the analysis of M1/M2 marker expression, but it was able to modify cell signaling pathways toward a dendritic cell-like pattern. Therefore, the present data suggest that TAM demonstrate plasticity toward dendritic cell-like signal transduction patterns, and that the alteration of the tumor microenvironment has the potential to reverse the immunosuppressive properties of TAM.
Tárgyszavak:Orvostudományok Egészségtudományok idegen nyelvű folyóiratközlemény külföldi lapban
tumor-associated macrophages
granulocyte-macrophage colony stimulating factor
macrophage colony stimulating factor receptor
cell signaling
Megjelenés:International Journal Of Oncology 38 : 5 (2011), p. 1409-1419. -
További szerzők:Saio, Masanao Gotoh, Naoe Umemura, Naoki Nonaka, Kenichi Bai, Juncheng Vízkeleti Laura (1984-) (molekuláris biológus, genetikus) Töröcsik Dániel (1979-) (bőrgyógyász) Balázs Margit (1952-) (sejtbiológus, molekuláris genetikus) Ádány Róza (1952-) (megelőző orvostan és népegészségtan szakorvos) Takami, Tsuyoshi
Internet cím:DOI
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