Abstracts from the 2009 Joint Meeting of the Society for Neuro-Oncology (SNO) and the American Association of Neurological Surgeons/Congress of Neurological Surgeons (AANS/CNS) Section on Tumors

摘要

Activation of the JNK pathway has been implicated in glioblastoma multiforme (GBM). Expression and activity of a specific JNK isoform, JNK2α2, are increased in 86% of primary GBMs. Since we have shown JNK2α2 is constitutively active and induces glial tumor formation, we studied the connection between JNK2α2 and a proto-oncogene, BCL-2. BCL-2 was the first gene associated with regulating apoptosis and is important for GBM cell survival. The JNK family was shown to directly phosphorylate BCL-2 at Ser70, thereby regulating its antiapoptotic ability. Enhanced phosphorylation of Ser70 increased resistance to apoptosis and increased tumor formation. We hypothesized that JNK2α2-induced tumorigenesis may result from altered levels of BCL-2 Ser70 phosphorylation.