Glioblastoma (GBM) is the most aggressive and prevalent primary malignancy of the central nervous system. S-Gboxin, a functional analog of gboxin, specifically inhibits primary mouse and human GBM cell growth with an IC50 value of 470 nM. Antitumor activity was first assessed by daily S-Gboxin treatment at 10 mg/kg/day beginning on day 3 or day 14 after mouse GBM (HTS cells) allograft flank implantation. S-Gboxin treated mice showed reduced tumor volume, cellular density, proliferation, and enhanced survival in comparison to vehicle controls. S-Gboxin treated tumors had reduced expression of the high-grade glioma makers, GFAP and Olig2. Primary human GBM cells were also injected into flanks of immunocompromised mice in the presence of matrigel. After visible tumors were detected (3 days) S-Gboxin was administered daily (10 mg/kg/day) resulting in significant attenuation of growth and decreased cellular density compared to controls. Further, S-Gboxin treatment (2.16 μg/day/mouse) inhibited tumor growth as manifested by reduced hemorrhaging, cellular density, and decreased proliferation. Histopathology analysis further showed reduced expression of the high-grade glioma makers. Moreover, S-Gboxin demonstrated inhibition of GBM PDX growth as manifested by general health status, reduced cellular density, cellular proliferation, and GBM marker expression[1].
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