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Induction of differentiation in k562 cell line by nicotinic acid-related compounds.
Ida, Chieri; Ogata, Shin; Okumura, Katsuzumi; Taguchi, Hiroshi.
Afiliação
  • Ida C; Laboratory of Molecular and Cellular Biology, Graduate School of Bioresources, Mie University.
Biosci Biotechnol Biochem ; 73(1): 79-84, 2009 Jan.
Article em En | MEDLINE | ID: mdl-19129652
Nicotinic acid and nicotinamide belong to the water-soluble vitamins, and they have many physiological and pharmacological functions in various organisms. In this study, we investigated the differentiation-inducing ability of nicotinic acid-related compounds in chronic myelogenous leukemia K562 cell line. Proliferation of K562 leukemia cells was inhibited by several nicotinic acid-related compounds. Hemoglobin content was increased by nicotinic acid and by isonicotinic acid. Isonicotinic acid increased gamma-globin mRNA expression as much as sodium butyrate did. The nuclei of nicotinic acid and of isonicotinic acid-treated cells decreased in size and the chromatin became more condensed. It was verified that nicotinic acid and isonicotinic acid induced erythroid differentiation in K562 cells. Expression of glycophorin A was increased by sodium butyrate. In contrast, it was decreased by nicotinic acid and by isonicotinic acid, suggesting that these compounds differentiate K562 to erythrocytes through different pathways than sodium butyrate does. Our data perhaps provide useful information as to the mechanisms of cell differentiation.
Assuntos
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Diferenciação Celular / Ácidos Nicotínicos Limite: Humans Idioma: En Revista: Biosci Biotechnol Biochem Assunto da revista: BIOQUIMICA / BIOTECNOLOGIA Ano de publicação: 2009 Tipo de documento: Article
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Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Diferenciação Celular / Ácidos Nicotínicos Limite: Humans Idioma: En Revista: Biosci Biotechnol Biochem Assunto da revista: BIOQUIMICA / BIOTECNOLOGIA Ano de publicação: 2009 Tipo de documento: Article