The median survival of glioblastoma (GBM) patients with HIV is significantly shorter compared to HIV-negative GBM patients, despite the fact that they receive the same treatments. This indicates that HIV infection is associated with more aggressive tumor behavior. Earlier we shown that gp120, a glycoprotein found in the HIV shell, stimulates up-regulation of glycolysis in glioma cells. The purpose of this study was to evaluate the underlying signaling mechanisms of gp120 dependent up-regulation of glycolysis in glioma cells.

Using antibody array and western blot we have identified that U87 glioma cells treated with gp120 (200 ng/ml) for 5 consequent days showed increased activation of MAP kinase and Akt/mTOR pathways. Increase of pAkt(pS473), pGSK3b(pS9), pMKK3(S189), pmTOR(S2448), p38(T180/Y182), pJNK(T183) has been identified. This data coincides with previously obtained results showing that glioma cells treated with gp120 exhibit higher proliferation rates and increased cell survival compared to un-treated glioma cells.

In summary, we conclude that gp120 triggers activation of regulatory kinases Akt and MAPK involved in cell growth, cell proliferation, cell survival, protein synthesis, transcription, glycolysis, and cell migration.

Citation Format: Gabriel Valentin-Guillama, Yuriy Kucheryavykh, Lilia Kucheryavykh. HIV-1 envelope protein gp120 promotes glioma tumor growth through the Akt and MAP kinase pathways [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 3454.