Exogenous Overexpression of P۵۳ with IFNγ Confer Synergistic Detrimental Impact on U۸۷

Introduction: Gliomas possess low immunogenicity which is an inevitable hinder in front of immunotherapy treatment. Interferon gamma (IFNγ) is a modulatory cytokine and the only member of type II interferon family. It is depicted that it has immune regulatory/modulatory activity, as well as anti-tumor properties. On the other hand it is reported that this protein may has a demon side, in this context IFNγ surprisingly acts as a tumor-progression agent partially because of its pro- inflammatory property.Methods: Here we aimed to examine the apoptotic characteristics of IFNγ on a Glioblastoma multiform cell line; we further investigated whether exogenous overexpression of P۵۳ has positive correlation with IFNγ treatment. P۵۳ expressing vector was amplified by E. coli BL۲۱. This vector confirmed by the aid of sequencing. At the next step U۸۷ cells were transfected using lipofectamin. Cells were treated rather by P۵۳ vector or and/or IFNγ .The kind of cellular death investigated by flow cytometery and the expression level of P۵۳ protein also precisely demonstrated by western blotting.Results: Sequencing results revealed that inserted P۵۳ was identical with human P۵۳. Western blot results revealed that IFNγ can up-regulate P۵۳ protein expression in this cell line.Conclusion: Interestingly, flow cytometry data determined that concurrent treatment with P۵۳ exogenous overexpression and IFNγ induces about ۷۰% apoptosis in U۸۷; more than the sum of cell death occurs after IFNγ or P۵۳ overexpression alone (~۱۸%+۲۱%=۳۹%). Results propose that IFNγ together with overexpression of P۵۳ exerts high anti-tumor activity in U۸۷ glioblastoma multiform.

کلیدواژه ها:

U۸۷ ، Glioblastoma ، poor immunogenic ، IFNγ ، P۵۳ over expression