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Provedor de dados:  Anais da ABC (AABC)
País:  Brazil
Título:  Inhibitory Effect on the Hepatitis B Cells through the Regulation of miR-122-MAP3K2 signal pathway
Autores:  CHEN,SONGLIN
YANG,LEI
PAN,AIPING
DUAN,SILIANG
LI,MINGFEN
LI,PING
HUANG,JINGJING
GAO,XINGXIN
HUANG,XIAOQI
LIN,YINGHUI
Data:  2019-01-01
Ano:  2019
Palavras-chave:  Hepatitis B cells
MiR-122
Inhibit
Signaling pathway
Resumo:  Abstract: The aim of this study was to investigate the inhibitory effect of regulation of miR-122-MAP3K2 signal pathway on the hepatitis B cells. We detected the content of MAP3K2 from patients with HBV blood serum samples and analyzed the correlation between content of MAP3K2 and copies of HBV-DNA. Wound healing and Transwell assays were used to detect the function of cells from control group (wild type) and observer group (overexpresses miR-122). Secretion levels of HBsAg and MAP3K2 in the supernatant and level of MAP3K2 in cells were detected by ELISA and western blot, respectively. The results showed that there was a positive correlation between the copies of HBV-DNA and MAP3K2 in serum. In the assays involving detection of the number of HBV-DNA copies, the supernatant levels of HBsAg and MAP3K2, and the level of MAP3K2 in the cells, the rate of increase of these indicators significantly slowed as culture time. In conclusion, overexpression of miR-122 could inhibit the migration of hepatoblastoma cells; however, following transfection with miR-122, DNA synthesis and the secretion of HBsAg were inhibited. Overexpression of miR-122 can also downregulate MAP3K2. Consequently, we concluded that regulating the miR-122-MAP3K2 signaling pathway exerts an inhibitory effect in hepatitis B cells.
Tipo:  Info:eu-repo/semantics/article
Idioma:  Inglês
Identificador:  http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0001-37652019000300703
Editor:  Academia Brasileira de Ciências
Relação:  10.1590/0001-3765201920180941
Formato:  text/html
Fonte:  Anais da Academia Brasileira de Ciências v.91 n.2 2019
Direitos:  info:eu-repo/semantics/openAccess
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