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Asian Pac J Cancer Prev ; 15(4): 1757-62, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24641404

RESUMO

Development of drugs from natural products has been undergoing a gradual evoluation. Many plant derived compounds have excellent therapeutic potential against various human ailments. They are important sources especially for anticancer agents. A number of promising new agents are in clinical development based on their selective molecular targets in the field of oncology. D-pinitol is a naturally occurring compound derived from soy which has significant pharmacological activitites. Therefore we selected D-pinitol in order to evaluate apoptotic potential in the MCF-7 cell line. Human breast cancer cells were treated with different concentrations of D-pinitol and cytotoxicity was measured by MTT and LDH assays. The mechanism of apoptosis was studied with reference to expression of p53, Bcl-2, Bax and NF-kB proteins. The results revealed that D-pinitol significantly inhibited the proliferation of MCF-7 cells in a concentration-dependent manner, while upregulating the expression of p53, Bax and down regulating Bcl-2 and NF-kB. Thus the results obtained in this study clearly vindicated that D-pinitol induces apotosis in MCF-7 cells through regulation of proteins of pro- and anti-apoptotic cascades.


Assuntos
Apoptose/efeitos dos fármacos , Neoplasias da Mama/tratamento farmacológico , Inositol/análogos & derivados , Proteína Supressora de Tumor p53/biossíntese , Proteína X Associada a bcl-2/biossíntese , Antineoplásicos/farmacologia , Neoplasias da Mama/patologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Fragmentação do DNA/efeitos dos fármacos , Feminino , Regulação Neoplásica da Expressão Gênica , Glutationa/biossíntese , Humanos , Inositol/farmacologia , L-Lactato Desidrogenase/metabolismo , Células MCF-7 , Preparações de Plantas/farmacologia , Proteínas Proto-Oncogênicas c-bcl-2/biossíntese , Glycine max/metabolismo , Fator de Transcrição RelA/biossíntese , Fator de Transcrição RelA/metabolismo
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