Aim: Search for key molecules to influence the tumor-targeted IFN-alpha2a-NGR anti-tumor sensitivity through signaling pathway study. Try to enhance the antitumor efficacy of IFN-alpha2a-NGR.
Methods: MTT method was used to determine the growth inhibitory effects of IFN-alpha2a-NGR on A549 and MKN-45 cells. Flow cytometry and Western blot were employed to detect the expression of STAT1, p-STAT1, p53, OAS and SOCS1; SOCS1 gene knock down was carried out by synthesized siRNA.
Results: When stimulated with IFN-alpha2a-NGR, the increased expression of STAT1, p-STAT1, p53, OAS and SOCS1 were observed in A549 cells, but only SOCS1 was notably increased in MKN-45 cells. The proliferation inhibition ability of MKN-45 to IFN-alpha2a-NGR was promoted by SOCS1 knocking down. (the inhibition rate was enhanced from 14.69%+/-1.05% to 36.97%+/-2.05%).
Conclusion: This study has further demonstrated that there were no differences on antitumor effects between IFN-alpha2a-NGR and IFN-alpha2a on cell or molecular level. Besides interferon-alpha receptor (IFNAR) which has been demonstrated before, p-STAT1, p53 and SOCS1 were important determinants of tumor resistance to IFNs therapy. The antitumor efficacy of IFN-alpha2a-NGR can be enhanced by RNA interference. These results might be helpful for the further development of IFN-alpha2a-NGR.
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Aim: Search for key molecules to influence the tumor-targeted IFN-alpha2a-NGR anti-tumor sensitivity through signaling pathway study. Try to enhance the antitumor efficacy of IFN-alpha2a-NGR.
Methods: MTT method was used to determine the growth inhibitory effects of IFN-alpha2a-NGR on A549 and MKN-45 cells.
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