Edited by Veli-Pekka LehtoKeywords: MicroRNAs miR-23b Liver regeneration Transforming growth factor-b1 Smad3 a b s t r a c t MicroRNAs (miRNAs) are known to play important roles in liver regeneration, although the role of miRNAs associated with the termination of liver regeneration is not as well studied. Here we reported the down-regulation of miR-23b in the termination stage of liver regeneration in rats. In addition, Smad3 was identified as a target of miR-23b during liver regeneration. Up-regulation of miR-23b promoted BRL-3A cell proliferation and partially inhibited transforming growth factor (TGF)-b1-induced apoptosis. Furthermore, TGF-b1 transcriptionally inhibited miR-23b expression. We conclude that down-regulation of miR-23b may contribute to activation of the TGF-b1/Smad3 signalling pathway during the termination stage of liver regeneration.
This study aimed to investigate the association of Epstein-Barr virus (EBV) with nuclear respiratory factor 1 (NRF1) and the biological function of NRF1 in EBV-associated gastric cancer (EBVaGC).
MethodsWestern blot and qRT-PCR were used to assess the effect of latent membrane protein 2A (LMP2A) on NRF1 expression after transfection with LMP2A plasmid or siLMP2A. The effects of NRF1 on the migration and apoptosis ability of GC cells were investigated by transwell assay and ow cytometry apoptosis analysis in vitro, respectively. In addition, we determined the regulatory role of NRF1 in EBV latent infection by western blot and droplet digital PCR (ddPCR).
ResultsLMP2A upregulated NRF1 expression by activating the NF-κB pathway. Moreover, NRF1 upregulated the expression of N-Cadherin and ZEB1 to promote cell migration. NRF1 promoted the expression of Bcl-2 to increase the anti-apoptosis ability of cells. In addition, NRF1 maintained latent infection of EBV by promoting the expression of the latent protein Epstein-Barr nuclear antigen 1 (EBNA1) and inhibiting the expression of the lytic proteins.
ConclusionsOur data indicated the role of NRF1 in EBVaGC progression and the maintenance of EBV latent infection. This provided a new theoretical basis for further NRF1-based anti-cancer therapy.
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