Data/hora: 09/06/2024 07:43:26

Provedor de dados: | 56
País: | Brazil
Título: | Antiproliferative effect of urolithin A, the ellagic acid-derived colonic metabolite, on hepatocellular carcinoma HepG2.2.15 cells by targeting Lin28a/let-7a axis
Autores: | Qiu,Zhenpeng; Zhou,Junxuan; Zhang,Cong; Cheng,Ye; Hu,Junjie; Zheng,Guohua.
Data: | 2018-01-01
Ano: | 2018
Palavras-chave: | Urolithin A; Hepatocellular carcinoma; Lin28a; Let-7a; Cell proliferation; HBx.
Resumo: | An abnormality in the Lin28/let-7a axis is relevant to the progression of hepatitis B virus (HBV)-positive hepatocellular carcinoma (HCC), which could be a novel therapeutic target for this malignant tumor. The present study aimed to investigate the antiproliferative and anti-invasive effects of urolithin A in a stable full-length HBV gene integrated cell line HepG2.2.15 using CCK-8 and transwell assays. The RNA and protein expressions of targets were assessed by quantitative PCR and western blot, respectively. Results revealed that urolithin A induced cytotoxicity in HepG2.2.15 cells, which was accompanied by the cleavage of caspase-3 protein and down-regulation of Bcl-2/Bax ratio. Moreover, urolithin A suppressed the protein expressions of Sp-1, Lin28a, and Zcchc11, and elevated the expression of microRNA let-7a. Importantly, urolithin A also regulated the Lin28a/let-7a axis in transient HBx-transfected HCC HepG2 cells. Furthermore, urolithin A decelerated the HepG2.2.15 cell invasion, which was involved in suppressing the let-7a downstream factors HMGA2 and K-ras. These findings indicated that urolithin A exerted the antiproliferative effect by regulating the Lin28a/let-7a axis and may be a potential supplement for HBV-infected HCC therapy.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2018000700602
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/1414-431x20187220
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.51 n.7 2018
Fonte: | info:eu-repo/semantics/openAccess