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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Nitric oxide and interactions with reactive oxygen species in the development of melanoma, breast, and colon cancer: A redox signaling perspective

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Autor(es):
Monteiro, Hugo P. [1] ; Rodrigues, Elaine G. [2] ; Amorim Reis, Adriana K. C. [3] ; Longo, Jr., Luiz S. [4] ; Ogata, Fernando T. [1] ; Moretti, Ana I. S. [5] ; da Costa, Paulo E. [1] ; Teodoro, Ana C. S. [1] ; Toledo, Mayte S. [1] ; Stern, Arnold [6]
Número total de Autores: 10
Afiliação do(s) autor(es):
[1] Univ Fed Sao Paulo Campus Sao Paulo, Escola Paulista Med, Ctr Cellular & Mol Therapy CTCMol, Dept Biochem, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo Campus Sao Paulo, Escola Paulista Med, Dept Microbiol Immunol & Parasitol, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo Campus Diadema, Inst Environm Chem & Pharmaceut Sci, Dept Chem, Diadema - Brazil
[4] Univ Fed Sao Paulo Campus Diadema, Inst Environm Chem & Pharmaceut Sci, Dept Pharmaceut Sci, Diadema - Brazil
[5] Univ Sao Paulo, Fac Med, Heart Inst, Lab Vasc Biol, Sao Paulo - Brazil
[6] NYU, Sch Med, New York, NY - USA
Número total de Afiliações: 6
Tipo de documento: Artigo Científico
Fonte: NITRIC OXIDE-BIOLOGY AND CHEMISTRY; v. 89, p. 1-13, AUG 1 2019.
Citações Web of Science: 1
Resumo

Cancer development is closely related to chronic inflammation, which is associated with identifiable markers of tumor progression, such as uncontrolled cell proliferation, angiogenesis, genomic instability, chemotherapeutic resistance, and metastases. Redox processes mediated by reactive oxygen species (ROS) and nitric oxide (NO) within the inflammatory tumor microenvironment play an essential role in directly influencing intercellular and intracellular signaling. These reactive species originating in the cancer cell or its microenvironment, mediate the epithelial-mesenchymal transition (EMT) and the mesenchymal-epithelial transition (MET). However, intracellular interactions between NO and ROS must be controlled to prevent cell death. Melanoma, breast, and colon cancer cells have developed a mechanism to survive and adapt to oxidative and nitrosative stress. The mechanism involves a spatial-temporal fine adjustment of the intracellular concentrations of NO and ROS, thereby guaranteeing the successful development of cancer cells. Physiological concentrations of NO and supra physiological concentrations of ROS are prevalent in cancer cells at the primary site. The situation reverses in cancer cells undergoing the EMT prior to being released into the blood stream. Intracellular supra physiological concentrations of NO found in circulating cancer cells endow them with anoikis resistance. When the anoikis-resistant cancer cells arrive at a metastatic site they undergo the MET. Endogenous supra physiological concentrations of ROS and physiological NO concentrations are prevalent in these cells. Understanding tumor progression from the perspective of redox signaling permits the characterization of new markers and approaches to therapy. The synthesis and use of compounds with the capacity of modifying intracellular concentrations of NO and ROS may prove effective in disrupting a redox homeostasis operative in cancer cells. (AU)

Processo FAPESP: 12/10470-1 - O papel do óxido nítrico e da enzima óxido nítrico sintase induzível na progressão de tumores humanos de cólon
Beneficiário:Hugo Pequeno Monteiro
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 13/16644-4 - S-nitrosotióis derivados de Aril-amidas e Aril-pirimidin-2-onas(tionas) - potenciais inibidores duplos de HIV-1-PR e renina: síntese, análise estrutural e ensaios biológicos
Beneficiário:Adriana Karla Cardoso Amorim Reis
Linha de fomento: Auxílio à Pesquisa - Regular
Processo FAPESP: 16/06539-7 - Avaliação de parâmetros inflamatórios e de estresse nitrosativo durante o desenvolvimento tumoral em ambiente hiperglicêmico
Beneficiário:Elaine Guadelupe Rodrigues
Linha de fomento: Auxílio à Pesquisa - Regular