Glioblastoma multiforme afflicts 12,500 new patients in the U.S. annually (Friedman et al., 2000; Stupp et al., 2009; Silber et al., 2012). Glioblastoma (GBM) is highly lethal, and the average survival expectancy is 14.6 months, and the overall 5-year survival rate for GBM is only 9.8% (Friedman et al., 2000; Stupp et al., 2009). High levels of resistance to current therapeutic modalities and cancer relapse are frequently seen in patients (Haar et al., 2012; Happold et al., 2012). The current standard therapy for GBM mainly includes maximum debulking surgery, radiation, and treatment with the monofunctional alkylating agent temozolomide (TMZ) (Friedman et al., 2000; Nishikawa, 2010). Multiple mechanisms are involved in the TMZ resistance, which may include cancer stem cells, microRNAs, drug efflux, DNA damage repair, tumor cells under hypoxia, histone deacetylation, epithelial-mesenchymal transition, STAT3 kinase, and many others (Haar et al., 2012; Happold et al., 2012; Johannessen and Bjerkvig, 2012; Kitange et al., 2012; Kohsaka et al., 2012; Zhang et al., 2012b).