Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 4 de 4
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
3.
Oncogene ; 35(18): 2357-69, 2016 05 05.
Artigo em Inglês | MEDLINE | ID: mdl-26279304

RESUMO

ZNF322A encoding a classical Cys2His2 zinc finger transcription factor was previously revealed as a potential oncogene in lung cancer patients. However, the oncogenic role of ZNF322A and its underlying mechanism in lung tumorigenesis remain elusive. Here we show ZNF322A protein overexpression in 123 Asian and 74 Caucasian lung cancer patients. Multivariate Cox regression analysis indicated that ZNF322A was an independent risk factor for a poor outcome in lung cancer, corroborating the Kaplan-Meier results that patients with ZNF322A protein overexpression had significantly poorer overall survival than other patients. Overexpression of ZNF322A promoted cell proliferation and soft agar growth by prolonging cell cycle in S phase in multiple lung cell lines, including the immortalized lung cell BEAS-2B. In addition, ZNF322A overexpression enhanced cell migration and invasion, whereas knockdown of ZNF322A reduced cell growth, invasion and metastasis abilities in vitro and in vivo. Quantitative proteomic analysis revealed potential ZNF322A-regulated downstream targets, including alpha-adducin (ADD1), cyclin D1 (CCND1), and p53. Using luciferase promoter activity assay combined with site-directed mutagenesis and sequential chromatin immunoprecipitation-PCR assay, we found that ZNF322A could form a complex with c-Jun and cooperatively activate ADD1 and CCND1 but repress p53 gene transcription by recruiting differential chromatin modifiers, such as histone deacetylase 3, in an AP-1 element dependent manner. Reconstitution experiments indicated that CCND1 and p53 were important to ZNF322A-mediated promotion of cell proliferation, whereas ADD1 was necessary for ZNF322A-mediated cell migration and invasion. Our results provide compelling evidence that ZNF322A overexpression transcriptionally dysregulates genes involved in cell growth and motility therefore contributes to lung tumorigenesis and poor prognosis.


Assuntos
Proteínas de Ligação a Calmodulina/genética , Ciclina D1/genética , Proteínas de Ligação a DNA/metabolismo , Neoplasias Pulmonares/metabolismo , Neoplasias Pulmonares/patologia , Fatores de Transcrição/metabolismo , Transcrição Gênica , Proteína Supressora de Tumor p53/genética , Idoso , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , Cromatina/genética , Feminino , Humanos , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Neoplasias Pulmonares/diagnóstico , Neoplasias Pulmonares/genética , Masculino , Pessoa de Meia-Idade , Metástase Neoplásica , Prognóstico , Regiões Promotoras Genéticas/genética , Fator de Transcrição AP-1/metabolismo
4.
Hunan Yi Ke Da Xue Xue Bao ; 24(3): 296-8, 1999.
Artigo em Chinês | MEDLINE | ID: mdl-12016813

RESUMO

Chlorine dioxide is a new type of forceful disinfectant, but it cannot be stored and transported as a gas and is very toxic. In this paper, a stable unified disinfectant capable of releasing chlorine dioxoide was introduced. This disinfectant was stable in dry state and could produce chlorine dioxide when it contacted with water. Its solution containing 3.3 mg.L-1 chlorine dioxide could kill 100% of B. subtilis var. niger spores after exposure for 5 minutes. Its solution containing 434 mg.L-1 chlorine dioxide could destroy 100% of HBsAg after exposure for 30 minutes. The content of chlorine dioxide in this disinfectant powder decreased by about 12% following storage at 56 degrees C for 14 days. It was essentially non-corrosive to stainless steel and moderately corrosive to carbon steel.


Assuntos
Compostos Clorados , Desinfetantes , Óxidos , Animais , Estabilidade de Medicamentos , Feminino , Humanos , Masculino , Ratos
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...