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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Nutritional shortage augments cisplatin-effects on murine melanoma cells

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Antunes, F. [1] ; Pereira, G. J. [1] ; Jasiulionis, M. G. [1] ; Bincoletto, C. [1] ; Smaili, S. S. [1]
Total Authors: 5
[1] Univ Fed Sao Paulo, EPM, Dept Pharmacol, UNIFESP, Rua Tres Maio 100, BR-04044020 Sao Paulo, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Chemico-Biological Interactions; v. 281, p. 89-97, FEB 1 2018.
Web of Science Citations: 3

Melanoma incidence increases every year worldwide and is responsible for 80% of skin cancer deaths. Due to its metastatic potential and resistance to almost any treatments such as chemo, radio, immune and targeted-therapy, the patients still have a poor prognosis, especially at metastatic stage. Considering that, it is crucial to find new therapeutic approaches to overcome melanoma resistance. Here we investigated the effect of cisplatin (CDDP), one of the chemotherapeutic agents used for melanoma treatment, in association with nutritional deprivation in murine melanoma cell lines. Cell death and autophagy were evaluated after the treatment with cisplatin, nutritional deprivation and its association using an in vitro model of murine melanocytes malignant transformation to metastatic melanoma. Our results showed that nutritional deprivation augmented cell death induced by cisplatin in melanoma cells, especially at the metastatic subtype, with slight effects on melanocytes. Mechanistic studies revealed that although autophagy was present at high levels in basal conditions in melanoma cells, was not essential for cell death process that involved mitochondrial damage, reactive oxygen species production and possible glycolysis inhibition. In conclusion, nutritional shortage in combination with chemotherapeutic drugs as cisplatin can be a valuable new therapeutic strategy to overcome melanoma resistance. (AU)

FAPESP's process: 12/51215-4 - Autophagy and glycogen synthase kinase-3 (GSK3) as molecular targets capable of increasing the activity of drugs used in the treatment of myeloid leukemias (acute and chronic)
Grantee:Claudia Bincoletto Trindade
Support type: Regular Research Grants
FAPESP's process: 13/20073-2 - Autophagy as a protective mechanism in senescent rats
Grantee:Soraya Soubhi Smaili
Support type: Regular Research Grants