Volume 19 Issue 2
Feb.  2021
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WANG Qiang-hua, PANG Qing, WANG Xue-gu, WU Hua, CHEN Hui-juan, ZHAO Wen-jun, LI Xiang. The role of PI3K/ Akt signaling pathway in upregulation of ISG15 induced by interferon 2α in hepatocellular carcinoma cells[J]. Chinese Journal of General Practice, 2021, 19(2): 182-185, 269. doi: 10.16766/j.cnki.issn.1674-4152.001762
Citation: WANG Qiang-hua, PANG Qing, WANG Xue-gu, WU Hua, CHEN Hui-juan, ZHAO Wen-jun, LI Xiang. The role of PI3K/ Akt signaling pathway in upregulation of ISG15 induced by interferon 2α in hepatocellular carcinoma cells[J]. Chinese Journal of General Practice, 2021, 19(2): 182-185, 269. doi: 10.16766/j.cnki.issn.1674-4152.001762

The role of PI3K/ Akt signaling pathway in upregulation of ISG15 induced by interferon 2α in hepatocellular carcinoma cells

doi: 10.16766/j.cnki.issn.1674-4152.001762
Funds:

 2008085J37

 BYKY18111

  • Received Date: 2020-10-16
    Available Online: 2022-02-19
  •   Objective  To investigate the mechanism of protein expression of interferon-stimulated gene 15 (ISG15) induced by interferon 2α (IFN-2α) via phosphatidy linositol 3-kinase (PI3K)/protein kinase B (Akt) in hepatocellular carcinoma cells.  Methods  HepG2 cells were cultured in the media containing IFN-2α and/or PI3K inhibitor LY294002, and four groups were created: control, IFN-2α, LY294002, IFN-2α+LY294002. The protein expressions of Akt, p-Akt and ISG15 were determined using western blot. Immunofluorescence was used to determine the co-expression of p-Akt and ISG15. Data were analyzed with one-way ANOVA followed by Bonferroni post hoc tests.  Results  Western blot analysis showed that the protein expression of ISG 15 was significantly increased in the IFN-2α group compared with control and IFN-2α+LY294002 group. Immunostaining analysis showed that the fluorescence intensity of ISG15 in the IFN-2α group was significantly higher than that in control and IFN-2α+LY294002 group. Western blot analysis showed that, in the IFN-2α group, the level of p-Akt (Thr308) was significantly increased, while the p-Akt (Ser473) was significantly decreased, compared with control group. Immunofluorescence results showed that the fluorescence intensity of p-Akt (Thr308) in the IFN-2α group was significantly higher than that in the control group and the IFN-2α+LY294002 group.  Conclusion  In HepG2 cells, IFN-2α induces the protein expression of ISG 15 via increasing p-Akt (Thr308) in the PI3K/Akt pathway.

     

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