Up-regulation of major histocompatibility complex class I-related molecules A (MICA) induced by 5-aza-2'-deoxycytidine / 中华肝脏病杂志
Chinese Journal of Hepatology
;
(12): 675-678, 2009.
Artigo
em Chinês
| WPRIM
| ID: wpr-306704
ABSTRACT
<p><b>OBJECTIVE</b>Major histocompatibility complex class I C-related molecules A and B (MICA and MICB) are innate immune system ligands for the NKG2D receptor expressed by natural killer cells and activated CD8(+)T cells. Our previous study showed that 5-aza-2'-deoxycytidine (5-aza-dC), a DNA methyltransferase inhibitor, can induce the expression of MICB and sensitized cells to NKL-cell-mediated cytolysis. The aim of this study was to determine the expression level of MICA in HepG2 cells (an HCC cell line) and L02 cells ( a normal liver cell), and to investigate the effect of 5-aza-dC on MICA expression in HepG2 cells.</p><p><b>METHODS</b>Cells were treated with 5-aza-dC, caffeine and ATM-specific siRNA. The cell surface MICA protein on HepG2 cells and L02 cells was determined using flow cytometry. The mRNA level was detected using real time RT-PCR.</p><p><b>RESULTS</b>MICA was undetectable on the surface of L02 cells, but was highly expressed on HepG2 cells. MICA expression was upregulated in response to 5-aza-dC treatment (P less than 0.05), and the upregulation of MICA was partially prevented by pharmacological or genetic inhibition of ataxia telangiectasia mutated (ATM) kinase (P less than 0.05).</p><p><b>CONCLUSION</b>Our data suggest that 5-aza-dC induces the expression of MICA by a DNA damage-dependent mechanism.</p>
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Azacitidina
/
Dano ao DNA
/
Cafeína
/
RNA Mensageiro
/
Antígenos de Histocompatibilidade Classe I
/
Regulação para Cima
/
Linhagem Celular
/
Membrana Celular
/
Proteínas Serina-Treonina Quinases
Limite:
Humanos
Idioma:
Chinês
Revista:
Chinese Journal of Hepatology
Ano de publicação:
2009
Tipo de documento:
Artigo
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