Articulatin-D induces apoptosis via activation of caspase-8 in acute T-cell leukemia cell line.
Mol Cell Biochem
; 426(1-2): 87-99, 2017 Feb.
Article
em En
| MEDLINE
| ID: mdl-27868169
ABSTRACT
Leukemia is among the most aggressive and prevalent human malignant carcinoma. Chemotherapy is the preferred therapeutic strategy; however, recurrence of cancer and non-selective cytotoxicity are the major concerns. Unlike synthetic chemotherapeutic agents, mistletoe ribosome-inactivating protein (RIP) displays anti-tumor function in various types of cancers. However, its effect on leukemia cells is little explored. In this study, we assessed the impact of Viscum articulatum RIP (Articulatin-D) on the survival of acute T-cell leukemia cells and the involved molecular and cellular mechanisms. Cell proliferation assay showed that Articulatin-D suppressed the viability of leukemia cells selectively. We further confirmed that the elevation of mitochondrial membrane potential and exposure of phosphatidylserine are the early events of apoptosis induction in Articulatin-D-treated Jurkat cells. Subsequently, we found that Articulatin-D treatment induces apoptosis in Jurkat cells in a time- and concentration-dependent manner. In conclusion, we provided evidence that Articulatin-D efficiently activates caspase-8 involved in extrinsic pathway of apoptosis induction, which ultimately results in caspase-3-dependent DNA fragmentation of Jurkat cells. Further evaluation of Articulatin-D in cell culture and animal models may provide novel information on selective cytotoxicity to acute T-cell leukemia and its involvement in targeting tumor cell survival pathways.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Toxinas Biológicas
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Apoptose
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Viscum
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Preparações de Plantas
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Proliferação de Células
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Caspase 8
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Leucemia-Linfoma Linfoblástico de Células T Precursoras
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Proteínas Inativadoras de Ribossomos Tipo 2
Limite:
Humans
Idioma:
En
Revista:
Mol Cell Biochem
Ano de publicação:
2017
Tipo de documento:
Article
País de afiliação:
Índia