scholarly journals Pigmentation Levels Affect Melanoma Responses to Coriolus versicolor Extract and Play a Crucial Role in Melanoma-Mononuclear Cell Crosstalk

2021 ◽  
Vol 22 (11) ◽  
pp. 5735
Author(s):  
Małgorzata Pawlikowska ◽  
Tomasz Jędrzejewski ◽  
Andrzej T. Slominski ◽  
Anna A. Brożyna ◽  
Sylwia Wrotek
Keyword(s):  
Cell Death ◽  
Melanoma Cell ◽  
Cell Response ◽  
Mononuclear Cells ◽  
Melanoma Cells ◽  
Coriolus Versicolor ◽  
Treatment Modalities ◽  
Cell Death Pathway ◽  
Fungus Extract ◽  
Tyrosine Concentration

Melanoma, the malignancy originating from pigment-producing melanocytes, is the most aggressive form of skin cancer and has a poor prognosis once the disease starts to metastasize. The process of melanin synthesis generates an immunosuppressive and mutagenic environment, and can increase melanoma cell resistance to different treatment modalities, including chemo-, radio- or photodynamic therapy. Recently, we have shown that the presence of melanin pigment inhibits the melanoma cell response to bioactive components of Coriolus versicolor (CV) Chinese fungus. Herein, using the same human melanoma cell line in which the level of pigmentation can be controlled by the L-tyrosine concentration in culture medium, we tested the effect of suppression of melanogenesis on the melanoma cell response to CV extract and investigated the cell death pathway induced by fungus extract in sensitized melanoma cells. Our data showed that susceptibility to CV-induced melanoma cell death is significantly increased after cell depigmentation. To the best of our knowledge, we are the first to demonstrate that CV extract can induce RIPK1/RIPK3/MLKL-mediated necroptosis in depigmented melanoma cells. Moreover, using the co-culture system, we showed that inhibition of the tyrosinase activity in melanoma cells modulates cytokine expression in co-cultured mononuclear cells, indicating that depigmentation of melanoma cells may activate immune cells and thereby influence a host anticancer response.

Coriolus versicolor ‐derived protein‐bound polysaccharides trigger the caspase‐independent cell death pathway in amelanotic but not melanotic melanoma cells

2019 ◽  
Vol 34 (1) ◽  
pp. 173-183 ◽  
Author(s):  
Małgorzata Pawlikowska ◽  
Jakub Piotrowski ◽  
Tomasz Jędrzejewski ◽  
Wiesław Kozak ◽  
Andrzej T. Slominski ◽  
...  
Keyword(s):  
Cell Death ◽  
Melanoma Cells ◽  
Coriolus Versicolor ◽  
Cell Death Pathway

scholarly journals Short Interfering RNA Directed against the SLUG Gene Increases Cell Death Induction in Human Melanoma Cell Lines Exposed to Cisplatin and Fotemustine

2007 ◽  
Vol 29 (4) ◽  
pp. 279-287
Author(s):  
Ivan Vannini ◽  
Massimiliano Bonafe ◽  
Anna Tesei ◽  
Marco Rosetti ◽  
Francesco Fabbri ◽  
...  
Keyword(s):  
Cell Death ◽  
Melanoma Cell ◽  
Melanoma Cells ◽  
Short Interfering Rna ◽  
Apoptotic Gene ◽  
Cycle Arrest ◽  
Therapeutic Protocols ◽  
Interfering Rna ◽  
New Strategies

Background: Melanoma remains largely resistant to currently available chemotherapy, and new strategies have been proposed to flank standardized therapeutic protocols in an effort to improve efficacy. Such an approach requires good knowledge of the mechanisms involved in the resistance and survival of melanoma cells. In this context, the SLUG gene has recently been characterized as a major regulator of melanocytes and melanoma cell survival. Methods: We tested the hypothesis that an oligonucleotide-based short interfering RNA (siRNA) directed against the SLUG gene increases the susceptibility of melanoma cells to drugs such as cisplatin and fotemustine, which are frequently used to treat this cancer. Results: It was found that SLUG siRNA increased cisplatin-induced cell death and rendered the drug active in vitro at half its plasmatic peak concentration. Such activity was correlated with an upregulation of the pro-apoptotic gene, PUMA. Furthermore, SLUG siRNA increased the capacity of fotemustine to elicit cell death and induced p21WAF1 upregulation, resulting in cell cycle arrest. Interestingly, this pathway did not require functional p53. Conclusion: These findings suggest that SLUG siRNA enhances the efficacy of two of the most widely used drugs to treat melanoma.

scholarly journals Mechanism for Regulation of Melanoma Cell Death via Activation of Thermo-TRPV4 and TRPV2

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Jiaojiao Zheng ◽  
Fangyuan Liu ◽  
Sha Du ◽  
Mei Li ◽  
Tian Wu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Cell Lines ◽  
Melanoma Cell ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Melanoma Cells ◽  
Human Malignant Melanoma ◽  
Transient Receptor ◽  
A375 Cells

Background. Thermo-TRPs (temperature-sensitive transient receptor potential channels) belong to the TRP (transient receptor potential) channel superfamily. Emerging evidence implied that thermo-TRPs have been involved in regulation of cell fate in certain tumors. However, their distribution profiles and roles in melanoma remain incompletely understood. Methods. Western blot and digital PCR approaches were performed to identify the distribution profiles of six thermo-TRPs. MTT assessment was employed to detect cell viability. Flow cytometry was applied to test cell cycle and apoptosis. Calcium imaging was used to determine the function of channels. Five cell lines, including one normal human primary epidermal melanocytes and two human malignant melanoma (A375, G361) and two human metastatic melanoma (A2058, SK-MEL-3) cell lines, were chosen for this research. Results. In the present study, six thermo-TRPs including TRPV1/2/3/4, TRPA1, and TRPM8 were examined in human primary melanocytes and melanoma cells. We found that TRPV2/4, TRPA1, and TRPM8 exhibited ectopic distribution both in melanocytes and melanoma cells. Moreover, activation of TRPV2 and TRPV4 could lead to the decline of cell viability for melanoma A2058 and A375 cells. Subsequently, activation of TRPV2 by 2-APB (IC50 = 150 μM) induced cell necrosis in A2058 cells, while activation of TRPV4 by GSK1016790A (IC50 = 10 nM) enhanced apoptosis of A375 cells. Furthermore, TRPV4 mediated cell apoptosis of melanoma via phosphorylation of AKT and was involved in calcium regulation. Conclusion. Overall, our studies revealed that TRPV4 and TRPV2 mediated melanoma cell death via channel activation and characterized the mechanism of functional TRPV4 ion channel in regulating AKT pathway driven antitumor process. Thus, they may serve as potential biomarkers for the prognosis and are targeted for the therapeutic use in human melanoma.

scholarly journals Caffeic Acid Phenethyl Ester Assisted by Reversible Electroporation—In Vitro Study on Human Melanoma Cells

Pharmaceutics ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 478
Author(s):  
Anna Choromanska ◽  
Jolanta Saczko ◽  
Julita Kulbacka
Keyword(s):  
Cell Death ◽  
Caffeic Acid ◽  
Melanoma Cell ◽  
Critical Role ◽  
Reactive Oxygen Species Generation ◽  
Caffeic Acid Phenethyl Ester ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Multi Drug Resistance ◽  
Reversible Electroporation

Melanoma is one of the most serious skin cancers. The incidence of this malignant skin lesion is continuing to increase worldwide. Melanoma is resistant to chemotherapeutic drugs and highly metastatic. Surgical resection can only be used to treat melanoma in the early stages, while chemotherapy is limited due to melanoma multi-drug resistance. The overexpression of glutathione S-transferase (GST) may have a critical role in this resistance. Caffeic acid phenethyl ester (CAPE) is a natural phenolic compound, which occurs in many plants. Previous studies demonstrated that CAPE suppresses the growth of melanoma cells and induces reactive oxygen species generation. It is also known that bioactivation of CAPE to its corresponding quinone metabolite by tyrosinase would lead to GST inhibition and selective melanoma cell death. We investigated the biochemical toxicity of CAPE in combination with microsecond electropermeabilization in two human melanoma cell lines. Our results indicate that electroporation of melanoma cells in the presence of CAPE induced high oxidative stress, which correlates with high cytotoxicity. Moreover, it can disrupt the metabolism of cancer cells by inducing apoptotic cell death. Electroporation of melanoma cells may be an efficient CAPE delivery system, enabling the application of this compound, while reducing its dose and exposure time.

scholarly journals Non-Apoptotic Cell Death Signaling Pathways in Melanoma

2020 ◽  
Vol 21 (8) ◽  
pp. 2980 ◽  
Author(s):  
Mariusz L. Hartman
Keyword(s):  
Cell Death ◽  
Signaling Pathways ◽  
Melanoma Cell ◽  
Apoptotic Cell ◽  
Genetic Alterations ◽  
Melanoma Cells ◽  
Apoptotic Cell Death ◽  
Specific Cell ◽  
Anti Cancer ◽  
Cell Death Signaling

Resisting cell death is a hallmark of cancer. Disturbances in the execution of cell death programs promote carcinogenesis and survival of cancer cells under unfavorable conditions, including exposition to anti-cancer therapies. Specific modalities of regulated cell death (RCD) have been classified based on different criteria, including morphological features, biochemical alterations and immunological consequences. Although melanoma cells are broadly equipped with the anti-apoptotic machinery and recurrent genetic alterations in the components of the RAS/RAF/MEK/ERK signaling markedly contribute to the pro-survival phenotype of melanoma, the roles of autophagy-dependent cell death, necroptosis, ferroptosis, pyroptosis, and parthanatos have recently gained great interest. These signaling cascades are involved in melanoma cell response and resistance to the therapeutics used in the clinic, including inhibitors of BRAFmut and MEK1/2, and immunotherapy. In addition, the relationships between sensitivity to non-apoptotic cell death routes and specific cell phenotypes have been demonstrated, suggesting that plasticity of melanoma cells can be exploited to modulate response of these cells to different cell death stimuli. In this review, the current knowledge on the non-apoptotic cell death signaling pathways in melanoma cell biology and response to anti-cancer drugs has been discussed.

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

A Cell Death Pathway Induced by Antibody-Mediated Cross-Linking of CD45 on Lymphocytes

2003 ◽  
Vol 23 (5-6) ◽  
pp. 421-440 ◽  
Author(s):  
Ann-Muriel Steff ◽  
Marylene Fortin ◽  
Fabianne Philippoussis ◽  
Sylvie Lesage ◽  
Chantal Arguin ◽  
...  
Keyword(s):  
Cell Death ◽  
Cross Linking ◽  
Cell Death Pathway ◽  
A Cell

Dynamical analysis of the programmed cell death pathway

2007 ◽  
Author(s):  
Luciano Carotenuto ◽  
Vincenza Pace ◽  
Dina Bellizzi ◽  
Giovanna De Benedictis
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Dynamical Analysis ◽  
Cell Death Pathway
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