pCramoll and rCramoll lectins induce cell death in human prostate adenocarcinoma (PC-3) cells by impairment of mitochondrial homeostasis

Autor(es)

Figueiroa, Evellyne de Oliveira ; Aranda-Souza, Mary Angela ; Varejao, Nathalia ; Rossato, Franco Aparecido ; Pereira Costa, Rute Alves ; Figueira, Tiago Rezende ; Nascimento da Silva, Luis Claudio ; Castilho, Roger Frigerio ; Vercesi, Anibal Eugenio ; dos Santos Correia, Maria Tereza

• Tipo de documento: Artigo Científico
• Fonte: TOXICOLOGY IN VITRO; v. 43, p. 40-46, SEP 2017.
• Citações Web of Science: 1

Resumo

Lectins from Cratylia molls seed have shown potential in vivo antitumor actions, however the mechanism have not yet been addressed. Here we evaluated the antitumor effects of native (pCramoll) and recombinant (rCramoll) lectins from C. mollis against human prostate adenocarcinoma (PC-3) cells. The viability of PC-3 cells was analyzed with the MIT assay and ANNEXIN V/propidium iodide staining. The actions of pCramoll or rCramoll on mitochondrial superoxide production, free cytosolic calcium concentration and mitochondrial membrane potential were evaluated using fluorescent probes (MitoSox Red, Fura 2-AM and safranin 0, respectively). pCramoll and rCramoll reduced the viability of PC-3 cells in a dose-dependent manner. Both lectins increased the generation of mitochondrial superoxide as well as the concentration of cytosolic calcium. These changes led to a decrease in oxidative phosphorylation, which impaired the formation of ATP. The resulting cell death was not blocked by MPT (mitochondrial permeability transition) inhibitors (Debio 025 or bongkrekic acid). Thus pCramoll and rCramoll promote PC-3 cell death through calcium signaling, leading to mitochondrial collapse. This work provides more insights into the action of pCramoll and rCramoll against cancer cells. These lectins represent valuable tools for biomedical research. (AU)

• Processo FAPESP: 11/51800-1 - Dano muscular induzido por exercício excêntrico: envolvimento da mitocôndria e interações com a miotoxicidade da estatina
• Beneficiário: Tiago Rezende Figueira
• Linha de fomento: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 11/50400-0 - Metabolismo energético, estado redox e funcionalidade mitocondrial na morte celular e em desordens cardiometabólicas e neurodegenerativas
• Beneficiário: Aníbal Eugênio Vercesi
• Linha de fomento: Auxílio à Pesquisa - Temático