scholarly journals Vascular Channel Formation by Human Melanoma Cells in Vivo and in Vitro: Vasculogenic Mimicry

1999 ◽  
Vol 155 (3) ◽  
pp. 739-752 ◽  
Author(s):  
Andrew J. Maniotis ◽  
Robert Folberg ◽  
Angela Hess ◽  
Elisabeth A. Seftor ◽  
Lynn M.G. Gardner ◽  
...  
Keyword(s):  
Vasculogenic Mimicry ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Channel Formation ◽  
Vascular Channel ◽  
Human Melanoma Cells

AMPK activation by GSK621 inhibits human melanoma cells in vitro and in vivo

2016 ◽  
Vol 480 (4) ◽  
pp. 515-521 ◽  
Author(s):  
Lezi Chen ◽  
Quan Chen ◽  
Guosan Deng ◽  
Shifeng Kuang ◽  
Jihong Lian ◽  
...  
Keyword(s):  
Melanoma Cells ◽  
Human Melanoma ◽  
Ampk Activation ◽  
Human Melanoma Cells

scholarly journals Treatment of melanoma cells with the synthetic retinoid CD437 induces apoptosis via activation of AP-1 in vitro, and causes growth inhibition in xenografts in vivo.

1996 ◽  
Vol 135 (6) ◽  
pp. 1889-1898 ◽  
Author(s):  
D Schadendorf ◽  
M A Kern ◽  
M Artuc ◽  
H L Pahl ◽  
T Rosenbach ◽  
...  
Keyword(s):  
Cell Death ◽  
Malignant Melanoma ◽  
Programmed Cell Death ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Mrna Levels ◽  
Synthetic Retinoid ◽  
Human Melanoma Cells

Human malignant melanoma is notoriously resistant to pharmacological modulation. We describe here for the first time that the synthetic retinoid CD437 has a strong dose-dependent antiproliferative effect on human melanoma cells (IC50: 5 x 10(-6) M) via the induction of programmed cell death, as judged by analysis of cell morphology, electron microscopical features, and DNA fragmentation. Programmed cell death was preceded by a strong activation of the AP-1 complex in CD437-treated cells as demonstrated by gel retardation and chloramphenicol transferase (CAT) assays. Northern blot analysis showed a time-dependent increase in the expression of c-fos and c-jun encoding components of AP-1, whereas bcl-2 and p53 mRNA levels remained constant. CD437 also exhibited a strong growth inhibitory effect on MeWo melanoma cells in a xenograft model. In tissue sections of CD437-treated MeWo tumors from these animals, apoptotic melanoma cells and c-fos overexpressing cells were colocalized by TdT-mediated deoxyuridine triphosphate-digoxigenin nick end labeling (TUNEL) staining and in situ hybridization. Taken together, this report identifies CD437 as a retinoid that activates and upregulates the transcription factor AP-1, leading eventually to programmed cell death of exposed human melanoma cells in vitro and in vivo. Further studies are needed to evaluate whether synthetic retinoids such as CD437 represent a new class of retinoids, which may open up new ways to a more effective therapy of malignant melanoma.

RETRACTED: A novel class of specific Hsp90 small molecule inhibitors demonstrate in vitro and in vivo anti-tumor activity in human melanoma cells

2011 ◽  
Vol 300 (1) ◽  
pp. 30-39 ◽  
Author(s):  
Pramod P. Mehta ◽  
Pei-Pei Kung ◽  
Shinji Yamazaki ◽  
Marlena Walls ◽  
Andrea Shen ◽  
...  
Keyword(s):  
Small Molecule ◽  
Small Molecule Inhibitors ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Human Melanoma Cells ◽  
Anti Tumor Activity

Suppression effect of a dual cancer-specific oncolytic adenovirus on luciferase-labeled human melanoma cells in vitro and in vivo

2021 ◽  
pp. 1-12
Author(s):  
Min Li ◽  
Yilong Zhu ◽  
Bing Bai ◽  
Jinbo Fang ◽  
Wei Yao ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Bioluminescence Intensity ◽  
Human Melanoma Cells ◽  
Related Proteins

BACKGROUND: To explore the suppressive effect of Apoptin-loaded oncolytic adenovirus (Ad-VT) on luciferase-labeled human melanoma cells in vitro and in vivo. METHODS: The stable luciferase-expressing human melanoma cells A375-luc or M14-luc were obtained by transfecting the plasmid pGL4.51 and selection with G418, followed by luciferase activity, genetic stability and bioluminescence intensity assays. In vitro, the inhibitory effects of Ad-VT on A375-luc or M14-luc were evaluated using the MTS cell proliferation, FITC-Annexin V apoptosis detection, transwell migration, Matrigel invasion and scratch assays. The inhibition pathway in Ad-VT-infected A375-luc and M14-luc cells were analyzed by JC-1 staining and Western-blot detection of mitochondrial apoptosis-related proteins. In vivo, the suppressive effects of Ad-VT on A375-luc or M14-luc were assessed by living imaging technology, tumor volume, bioluminescence intensity, survival curves and immunohistochemical analysis of the tumors from the xenograft tumor model BALB/c nude mice. RESULTS: The growth and migration of A375-luc and M14-luc were significantly inhibited by Ad-VT in vitro. The evaluations of A375-luc and M14-luc tumor models in BALB/c nude mice were successfully performed using living imaging technology. Ad-VT had an anti-tumor effect by reducing tumor growth and increasing survival in vivo. Ad-VT significantly changed the mitochondrial membrane potential by triggering the the mitochondrial release of apoptosis-related proteins, AIF (apoptosis inducing factor), ARTS (Apoptosis-Related Proteins), and Cyto-c (cytochrome c) from the mitochondria. CONCLUSION: Ad-VT reduced the mitochondrial membrane potential in A375-luc or M14-luc cells and induced the mitochondrial release of AIF, ARTS and Cyto-C. Ad-VT induced apoptosis in A375-luc or M14-luc cells via the mitochondrial apoptotic pathway.

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