scholarly journals Monensin may inhibit melanoma by regulating the selection between differentiation and stemness of melanoma stem cells

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7354 ◽  
Author(s):  
Haoran Xin ◽  
Jie Li ◽  
Hao Zhang ◽  
Yuhong Li ◽  
Shuo Zeng ◽  
...  
Keyword(s):  
Stem Cells ◽  
Drug Repurposing ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
High Rate ◽  
Chemotherapy Drugs ◽  
Human Melanoma Cells ◽  
Melanoma Treatment

Melanoma is the most lethal cutaneous malignancy that threatens human lives. Poor sensitivity to chemotherapy drugs and the high rate of resistance are the bottlenecks of melanoma treatment. Thus, new chemotherapy drugs are needed. Drug repurposing is a safe, economical and timesaving way to explore new chemotherapy for diseases. Here, we investigated the possibility of repurposing the antibiotic monensin as an anti-melanoma agent. Using three human melanoma cells and two nomal human cell lines as cell models, we found that monensin is obviously toxic to human melanoma cells while safe to nomal human cells. It effectively inhibited cell proliferation and viability, while promoted apoptosis and differentiation of human melanoma cells in vitro. By establishment of an animal model of transplanted human melanoma in nude mice, we demonstrated that monensin suppressed the growth of xenografts in vivo. At the same time, we found that melanogenesis increased and the ability of sphere and cloning forming of melanoma decreased under the treatment of monensin. Further detection about differentiation and pluripotent regulations were executed. Our results suggest that monensin is a potent inhibitor of melanoma, and its anti-tumor mechanism may be through promoting the final differentiation of melanoma stem cells and inhibiting their stemness maintenance.

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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