Melanoma Cell Viability Is Reduced after Endoglin Silencing with Gene Electrotransfer

2016 ◽  
pp. 325-328
Author(s):  
T. Dolinsek ◽  
G. Sersa ◽  
M. Cemazar
Keyword(s):  
Cell Viability ◽  
Melanoma Cell ◽  
Gene Electrotransfer

Ursolic acid and resveratrol synergize with chloroquine to reduce melanoma cell viability

2015 ◽  
Vol 25 (2) ◽  
pp. 103-112 ◽  
Author(s):  
Jacob J. Junco ◽  
Anna Mancha-Ramirez ◽  
Gunjan Malik ◽  
Sung-Jen Wei ◽  
Dae Joon Kim ◽  
...  
Keyword(s):  
Cell Viability ◽  
Ursolic Acid ◽  
Melanoma Cell

scholarly journals Intratumoral Gene Electrotransfer of Plasmid DNA Encoding shRNA against Melanoma Cell Adhesion Molecule Radiosensitizes Tumors by Antivascular Effects and Activation of an Immune Response

Vaccines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 135 ◽  
Author(s):  
Simona Kranjc Brezar ◽  
Valter Mrak ◽  
Masa Bosnjak ◽  
Monika Savarin ◽  
Gregor Sersa ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Melanoma Cell ◽  
Adhesion Molecule ◽  
Plasmid Dna ◽  
Cell Adhesion Molecule ◽  
Antitumor Effect ◽  
Combined Therapy ◽  
Gene Electrotransfer ◽  
Tumor Models ◽  
Melanoma Cell Adhesion Molecule

In this study, radiotherapy was combined with the gene electrotransfer (GET) of plasmid encoding shRNA against melanoma cell adhesion molecule (pMCAM) with dual action, which was a vascular-targeted effect mediated by the silencing of MCAM and an immunological effect mediated by the presence of plasmid DNA in the cytosol-activating DNA sensors. The effects and underlying mechanisms of therapy were evaluated in more immunogenic B16F10 melanoma and less immunogenic TS/A carcinoma. The silencing of MCAM potentiated the effect of irradiation (IR) in both tumor models. Combined therapy resulted in 81% complete responses (CR) in melanoma and 27% CR in carcinoma. Moreover, after the secondary challenge of cured mice, 59% of mice were resistant to challenge with melanoma cells, and none were resistant to carcinoma. Combined therapy reduced the number of blood vessels; induced hypoxia, apoptosis, and necrosis; and reduced cell proliferation in both tumor models. In addition, the significant increase of infiltrating immune cells was observed in both tumor models but more so in melanoma, where the expression of IL-12 and TNF-α was determined as well. Our results indicate that the combined therapy exerts both antiangiogenic and immune responses that contribute to the antitumor effect. However, tumor immunological status is crucial for a sufficient immune system contribution to the overall antitumor effect.

Tetrameric RGD induces clustering of integrin αvβ3 on the melanoma cell surface and decreases cell viability

2016 ◽  
Vol 71 (4) ◽  
pp. 227-235
Author(s):  
M. A. Rubtsov ◽  
A. A. Maslakova ◽  
D. M. Potashnikova ◽  
V. P. Veiko ◽  
M. S. Syrkina
Keyword(s):  
Cell Surface ◽  
Cell Viability ◽  
Melanoma Cell ◽  
Integrin Αvβ3

Role of AXL in metastatic melanoma and impact of TP-0903 as a novel therapeutic option for melanoma brain metastasis.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e22021-e22021
Author(s):  
Eemon Tizpa ◽  
Hannah J Young ◽  
Kimberley-Jane C. Bonjoc ◽  
Chou-Wei Chang ◽  
Yilun Liu ◽  
...  
Keyword(s):  
Overall Survival ◽  
Drug Resistance ◽  
Malignant Melanoma ◽  
Cell Viability ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Therapeutic Option ◽  
Poor Survival ◽  
Malignant Melanoma Cell ◽  
Melanoma Cell Lines

e22021 Background: Melanoma brain metastases (MBM) are common with a median overall survival of 4-5 months. Although immunotherapies have improved clinical outcomes and have doubled overall survival in MBM, there is a high incidence rate of relapse caused by drug resistance. AXL, a receptor tyrosine kinase (RTK), is associated with drug resistance and metastasis in many cancers. The activation of AXL via trans-phosphorylation regulates multiple signaling pathways that induce tumor survival, metastasis, drug resistance, and epithelial-to-mesenchymal transition (EMT). In MBM, AXL is upregulated and associated with disease progression, promoting cell invasion and migration. This suggests that targeting AXL can be a novel strategy to overcome treatment-related resistance in MBM. TP-0903, an investigational small molecule inhibitor of AXL, has shown efficacy in reversing the mesenchymal phenotype and re-sensitizing resistant cancer cells to targeted therapies in heme malignancies, pancreatic, and breast cancer. We aim to investigate the efficacy of TP-0903 in MBM. Methods: The Cancer Genome Atlas (TCGA) data was utilized to investigate the signaling pathways downstream of AXL that are upregulated in advanced melanoma. Nine signaling molecules including AKT1, mTOR, and PAK4 were analyzed to identify any correlation between gene expression levels and overall survival. Four metastatic melanoma cell lines were used to evaluate the effect of TP-0903 on cell viability and active AXL downregulation was assessed in vitro through MTS cell viability assays and Immunoblotting. Wound closure assays were executed to understand the functional consequences of AXL downregulation. Results: In all nine genes, high expression levels confer poor survival probability. Cell viability assays of four malignant melanoma cell lines showed that TP-0903 treatment resulted in IC50 values ranging from 32 – 692 nM. Western blot analysis indicated that TP-0903 reduced the levels of phosphorylated AXL in malignant melanoma cell lines. In addition, increasing TP-0903 concentrations reduced the rate of cell migration in these malignant melanoma cell lines. Conclusions: AXL plays a role in EMT, treatment resistance, and metastasis in MBM, resulting in poor survival. Our findings suggest TP-0903 is effective in reducing cell migration, inhibit metastasis, and can be a potential therapeutic option in MBM.

scholarly journals A Functional Screen Identifies Specific MicroRNAs Capable of Inhibiting Human Melanoma Cell Viability

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e43569 ◽  
Author(s):  
Jos B. Poell ◽  
Rick J. van Haastert ◽  
Thijs de Gunst ◽  
Iman J. Schultz ◽  
Willemijn M. Gommans ◽  
...  
Keyword(s):  
Cell Viability ◽  
Melanoma Cell ◽  
Human Melanoma ◽  
Human Melanoma Cell ◽  
Functional Screen

scholarly journals Bcl2 Regulation by the Melanocyte Master Regulator Mitf Modulates Lineage Survival and Melanoma Cell Viability

Cell ◽  
2002 ◽  
Vol 109 (6) ◽  
pp. 707-718 ◽  
Author(s):  
Gaël G. McGill ◽  
Martin Horstmann ◽  
Hans R. Widlund ◽  
Jinyan Du ◽  
Gabriela Motyckova ◽  
...  
Keyword(s):  
Cell Viability ◽  
Melanoma Cell ◽  
Master Regulator

scholarly journals The Impact of Olive Oil Compounds on the Metabolic Reprogramming of Cutaneous Melanoma Cell Models

Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 289
Author(s):  
Cheila Brito ◽  
Ana Tomás ◽  
Sandra Silva ◽  
Maria Rosário Bronze ◽  
Ana Teresa Serra ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Cell Viability ◽  
Olive Oil ◽  
Melanoma Cell ◽  
Cutaneous Melanoma ◽  
Melanoma Cells ◽  
Metabolic Reprogramming ◽  
Cytotoxic Potential ◽  
Erk Activation ◽  
Jnk Activation

Cutaneous melanoma is the deadliest type of skin cancer, characterized by a high molecular and metabolic heterogeneity which contributes to therapy resistance. Despite advances in treatment, more efficient therapies are needed. Olive oil compounds have been described as having anti-cancer properties. Here, we clarified the cytotoxic potential of oleic acid, homovanillyl alcohol, and hydroxytyrosol on melanoma cells. Metabolic viability was determined 48 h post treatment of A375 and MNT1 cells. Metabolic gene expression was assessed by qRT-PCR and Mitogen-Activated Protein Kinase (MAPK) activation by Western blot. Hydroxytyrosol treatment (100 and 200 µM) significantly reduced A375 cell viability (p = 0.0249; p < 0.0001) which, based on the expression analysis performed, is more compatible with a predominant glycolytic profile and c-Jun N-terminal kinase (JNK) activation. By contrast, hydroxytyrosol had no effect on MNT1 cell viability, which demonstrates an enhanced oxidative metabolism and extracellular signal-regulated kinase (ERK) activation. This compound triggered cell detoxification and the use of alternative energy sources in A375 cells, inhibiting JNK and ERK pathways. Despite oleic acid and homovanillyl alcohol demonstrating no effect on melanoma cell viability, they influenced the MNT1 glycolytic rate and A375 detoxification mechanisms, respectively. Both compounds suppressed ERK activation in MNT1 cells. The distinct cell responses to olive oil compounds depend on the metabolic and molecular mechanisms preferentially activated. Hydroxytyrosol may have a cytotoxic potential in melanoma cells with predominant glycolytic metabolism and JNK activation.

scholarly journals Analysis Of Candidate Genes Expected To Be Essential For Melanoma Surviving

2020 ◽  
Author(s):  
Irina Krivosheeva ◽  
Alexandra Filatova ◽  
Sergei Moshkovskii ◽  
Ancha Baranova ◽  
Mikhail Skoblov
Keyword(s):  
Cell Viability ◽  
Cell Line ◽  
Melanoma Cell ◽  
Melanoma Cell Line ◽  
Computational Models ◽  
Target Genes ◽  
The Other ◽  
Other Hand ◽  
Before And After

Abstract Cancers may be treated by selective targeting of the genes vital for their survival. A number of attempts have led to discovery of several genes essential for surviving of tumor cells of different types. In this work, we tried to analyze genes that were previously predicted to be essential for melanoma surviving. Here we present the results of transient siRNA-mediated knockdown of the four of such genes, namely, UNC45A, STK11IP, RHPN2 and ZNFX1, in melanoma cell line A375, then assayed the cells for their viability, proliferation and ability to migrate in vitro. In our study, the knockdown of the genes predicted as essential for melanoma survival does not lead to statistically significant changes in cell viability. On the other hand, for each of the studied genes, mobility assays showed that the knockdown of each of the target genes accelerates the speed of cells migrating. Possible explanation for such counterintuitive results may include insufficiency of the predicting computational models or the necessity of a multiplex knockdown of the genes.AimsTo examine the hypothesis of essentiality of hypomutated genes for melanoma surviving we have performed knockdown of several genes in melanoma cell line and analyzed cell viability and their ability to migrate.MethodsKnockdown was performed by siRNAs transfected by Metafectene PRO. The levels of mRNAs before and after knockdown were evaluated by RT-qPCR analysis. Cell viability and proliferation were assessed by MTT assay. Cell migration was assessed by wound healing assay.ResultsThe knockdown of the genes predicted as essential for melanoma survival does not lead to statistically significant changes in cell viability. On the other hand, for each of the studied genes, mobility assays showed that the knockdown of each of the target genes accelerates the speed of cells migrating. ConclusionOur results do not confirm initial hypothesis that the genes predicted essential for melanoma survival as a matter of fact support the survival of melanoma cells.

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