scholarly journals Anchorage independence altered vasculogenic phenotype of melanoma cells through downregulation in aminopeptidase N /syndecan-1/integrin β4 axis

Aging ◽  
2020 ◽  
Vol 12 (17) ◽  
pp. 16803-16819
Author(s):  
Yu-Che Cheng ◽  
Wei-Chi Ku ◽  
Ting-Ting Tseng ◽  
Ching-Po Wu ◽  
Mengjin Li ◽  
...  
Keyword(s):  
Melanoma Cells ◽  
Aminopeptidase N ◽  
Anchorage Independence ◽  
Integrin Β4

Sequential detection of mRNA for the chemokine IL-8 and macrophages (F4/80) in human melanoma

1995 ◽  
Vol 53 ◽  
pp. 1008-1009
Author(s):  
C.D. Bucana ◽  
R. Sanchez ◽  
R. Singh ◽  
I.J. Fidler
Keyword(s):  
Tumor Cells ◽  
Nude Mice ◽  
Constitutive Expression ◽  
Metastatic Potential ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Angiogenic Factor ◽  
Infiltrating Cells ◽  
Immunoperoxidase Assay ◽  
Multifunctional Cytokine

The purpose of this study was to demonstrate by ISH the presence of IL-8 mRNA, and by immunohistochemistry (IHC) the presence of the chemokine IL-8 and the distribution of infiltrating macrophages in subcutaneous melanomas in the same tumor. IL-8 is a multifunctional cytokine produced by melanoma cells, activated macrophages and monocytes and it has been shown to be a growth and angiogenic factor for tumor cells. More recently it was shown that constitutive expression of IL-8 correlated directly with metastatic potential of human melanoma cells in nude mice. IL-8 content of a solid tumor as determined by Western blot analysis does not take into account the contribution of macrophages. Previous studies showed that murine tumors contain many infiltrating cells interspersed among tumor cells whereas human tumors growing in nude mice exhibit macrophages at the periphery or between tumor islands. In this study we demonstrate the expression of IL-8 and the distribution of macrophages by immunoperoxidase assay and IL-8 mRNA by ISH.

Oleanolic acid rich solubilized triterpene extracts from mistletoe induce apoptotic and necrotic cell death of murine B16. F10 melanoma cells

Planta Medica ◽  
2009 ◽  
Vol 75 (09) ◽  
Author(s):  
CM Strüh ◽  
S Jäger ◽  
CM Schempp ◽  
T Jakob ◽  
A Scheffler ◽  
...  
Keyword(s):  
Cell Death ◽  
Oleanolic Acid ◽  
Melanoma Cells ◽  
Necrotic Cell Death ◽  
Necrotic Cell

Comparative gene expression study in WM164 melanoma cells treated with dimethylacrylshikonin.

2017 ◽  
Author(s):  
N Kretschmer ◽  
A Deutsch ◽  
B Rinner ◽  
M Scheideler ◽  
R Bauer
Keyword(s):  
Gene Expression ◽  
Melanoma Cells ◽  
Gene Expression Study ◽  
Expression Study

Ancylostoma caninum Anticoagulant Peptide Blocks Metastasis In Vivo and Inhibits Factor Xa Binding to Melanoma Cells In Vitro

1998 ◽  
Vol 79 (05) ◽  
pp. 1041-1047 ◽  
Author(s):  
Kathleen M. Donnelly ◽  
Michael E. Bromberg ◽  
Aaron Milstone ◽  
Jennifer Madison McNiff ◽  
Gordon Terwilliger ◽  
...  
Keyword(s):  
Active Site ◽  
Thrombin Generation ◽  
Factor Xa ◽  
Coagulation Factor ◽  
Melanoma Cells ◽  
Factor V ◽  
Ancylostoma Caninum ◽  
Metastatic Activity

SummaryWe evaluated the in vivo anti-metastatic activity of recombinant Ancylostoma caninum Anticoagulant Peptide (rAcAP), a potent (Ki = 265 pM) and specific active site inhibitor of human coagulation factor Xa originally isolated from bloodfeeding hookworms. Subcutaneous injection of SCID mice with rAcAP (0.01-0.2 mg/mouse) prior to tail vein injection of LOX human melanoma cells resulted in a dose dependent reduction in pulmonary metastases. In order to elucidate potential mechanisms of rAcAP’s anti-metastatic activity, experiments were carried out to identify specific interactions between factor Xa and LOX. Binding of biotinylated factor Xa to LOX monolayers was both specific and saturable (Kd = 15 nM). Competition experiments using antibodies to previously identified factor Xa binding proteins, including factor V/Va, effector cell protease receptor-1, and tissue factor pathway inhibitor failed to implicate any of these molecules as significant binding sites for Factor Xa. Functional prothrombinase activity was also supported by LOX, with a half maximal rate of thrombin generation detected at a factor Xa concentration of 2.4 nM. Additional competition experiments using an excess of either rAcAP or active site blocked factor Xa (EGR-Xa) revealed that most of the total factor Xa binding to LOX is mediated via interaction with the enzyme’s active site, predicting that the vast majority of cell-associated factor Xa does not participate directly in thrombin generation. In addition to establishing two distinct mechanisms of factor Xa binding to melanoma, these data raise the possibility that rAcAP’s antimetastatic effect in vivo might involve novel non-coagulant pathways, perhaps via inhibition of active-site mediated interactions between factor Xa and tumor cells.

Re-expression of Dipeptidylpeptidase 4 (DPP4) in melanoma cells – insights into molecular consequences

2004 ◽  
Vol 30 (08/09) ◽  
Author(s):  
B Becker ◽  
A Roesch ◽  
C Hafner ◽  
W Stolz ◽  
M Landthaler ◽  
...  
Keyword(s):  
Melanoma Cells ◽  
Dipeptidylpeptidase 4

Evaluation of radiation-induced genotoxicity on hu-man melanoma cells (SK-MEL-37) by flow cytometry

2019 ◽  
Vol 7 (2A) ◽  
Author(s):  
Leticia Bonfim ◽  
Luma Ramirez de Carvalho ◽  
Daniel Perez Vieira
Keyword(s):  
Genetic Material ◽  
Micronucleus Assay ◽  
Melanoma Cells ◽  
Dead Cell ◽  
Genotoxic Damage ◽  
Sytox Green ◽  
60Co Source ◽  
Radiation Induced ◽  
Death And Loss ◽  
Cell Fractions

Micronucleus assay is a test used to evaluate genotoxic damage in cells, which can be caused by various factors, like ionizing radiation. Interactions between radiation energies and DNA can cause breakage, leading to use chromosomal mutations or loss of genetic material, important events that could be induced in solid tumors to mitigate its expansion within human body.  Melanoma has been described as a tumor with increased radio resistance.  This work evaluated micronuclei percentages (%MN) in human melanoma cells (SK-MEL-37), irradiated by gamma radiation, with doses between 0 and 16Gy.  Cell suspensions were irradiated in PBS by a 60Co source in doses between 0 and 16Gy, and incubated by 48h.  Then cell membranes were lysed in the presence of SYTOX Green and EMA dyes, preserving nuclear membranes.  Using this method, EMA-stained nuclei could be discriminated as those derived from dead cells, and SYTOX nuclei and micronuclei could be quantified.  Micronuclei percentages were found to be proportional to dose, (R2 = 0.997).  Only the highest dose (16Gy) could induce statistically significant increase of MN (p<0.0001), although cultures irradiated by 4, 8 and 16Gy showed significant increase of dead cell fractions.  Calculation of the nuclei-to-beads ratio showed that 8 and 16Gy could reduce melanoma cell proliferation.  Results showed that although cell death and loss of proliferative capacity could be observed on cultures irradiated at lower doses, genotoxic damage could be induced only on a higher dose. Resistance to radiation-induced genotoxicity could explain a relatively high radio resistance of melanoma tumors.

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