Inhibitory effects of interferon b on XXXX HepG2 via Akt/STAT phosphorylation.

@entity137 @entity589 @entity588 @entity96 @entity5 @entity2391 @entity157
UNASSIGNED: Conventional chemotherapy fails to cure metastatic @entity157 mainly due to its high hepatotoxicity. Currently, doxorubicin is the most widely used drug against @entity96 either as single agent or in combination with other chemotherapeutics like cisplatin. It is limited due to their severe @entity137 on normal hepatocytes. Therefore, alternative therapeutic agents without or with low hepatotoxicity are highly desirable. Interferons are a family of cytokines that potently demonstrate antiviral, immunomodulatory and anti-proliferative activities. It also exerts direct cytotoxic effects on @entity5 cells. The purpose of this study was to examine the in vitro @entity137 of interferon b on HepG2 cells. We revealed the presence of binding receptor of interferon b in HepG2 cells. The dose-dependent inhibition on cell proliferation was observed. We demonstrated that @entity2391 exhibited significant @entity137 in HepG2 cells mainly through phosphorylation of signal transducers and activators of transcription2. The activation of Akt was suppressed. The stimulation of pro-apoptotic protein expression of @entity589 , inhibition of anti-apoptotic protein expression of @entity588 , activation of cleaved caspase 9 _ 3, was found at increasing concentrations. In conclusion, our results suggest that interferon b has potential to inhibit cell proliferation dose-dependently. Increased concentrations of interferon b influenced apoptosis via mitochondrial pathway through inhibition of p-Akt. This article is protected by copyright. All rights reserved.
