Glioblastoma multiforme is the most common type of brain cancer in adults, with current treatments yielding a 1-year prognosis for survival (Collins et. al., 2004). p53-mutation may contribute to resistance to apoptosis-inducing chemotherapy (Wetmore, 2000).  Alternative autophagy-inducing strategies, such as plumbagin and rapamycin are inhibitors of the PI3/Akt/mTOR pathway, a major cellular pathway that is activated in response to survival signals (Lefranc et. al., 2007). c-Jun N-terminal kinase (JNK), a member of the mitogen-activated protein MAP kinase family, can induce autophagy through P53 activation or through interaction with Beclin-1. The purpose of this research is to investigate the effect of p53-mutation on the occurrence of autophagy in p53-mutant U138MG and wild-type p53 U87MG glioblastoma cells in the presence of plumbagin, rapamycin and the JNK inhibitor, SP600125.

Impact of p53 on the occurrence of autophagy in <i>p53</i> mutant U138 cells and wild type <i>p53</i> U87 cells

243rd National Meeting (2012)

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.

Impact of p53 on the occurrence of autophagy in p53 mutant U138 cells and wild type p53 U87 cells