Aim： To examine the effects of anisomycin on glioma cells and the related mechanisms in vitro. Methods： The U251 and U87 human glioblastoma cell lines were tested. The growth of the cells was analyzed using a CCK-8 cell viability assay. Apoptosis was detected using a flow cytometry assay. The expression of proteins and phosphorylated kinases was detected using Western blotting. Results： Treatment of U251 and U87 cells with anisomycin （0.01-8 pmol/L） inhibited the cell growth in time- and concentration- dependent manners （the IC50 values at 48 h were 0.233±0.021 and 0.192±0.018 pmol/L, respectively）. Anisomycin （4 pmol/L） caused 21.5%±2.2% and 25.3%±3.1% of apoptosis proportion, respectively, in U251 and U87 cells. In the two cell lines, anisomycin （4 pmol/L） activated p38 MAPK and JNK, and inactivated ERK1/2. However, neither the p38 MAPK inhibitor SB203580 （10 pmol/L） nor the JNK inhibitor SP600125 （10μmol/L） prevented anisomycin-induced cell death. On the other hand, anisomycin （4 μmol/L） reduced the level of PP2A/C subunit （catalytic subunit） in a time-dependent manner in the two cell lines. Treatment of the two cell lines with the PP2A inhibitor okadaic acid （100 nmol/L） caused marked cell death. Conclusion： Anisomycin induces glioma cell death via down-regulation of PP2A catalytic subunit. The regulation of PP2A/C exression by anisomycin provides a clue to further study on its role in glioma therapy.