Contribution of autophagic cell death to p53-dependent cell death in human glioblastoma cell line SF126

Yasuhiro Sakamoto, Shunsuke Kato, Masahiro Takahashi, Yoshinari Okada, Katsuhiro Yasuda, Gou Watanabe, Hiroo Imai, Atsuko Sato, Chikashi Ishioka

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)


Apoptosis and autophagic cell death are programmed cell deaths that are involved in cell survival, growth, development and carcinogenesis. p53, the most extensively studied tumor suppressor, regulates apoptosis and autophagy by transactivating its downstream genes. It also stimulates the mitochondrial apoptotic pathway and inhibits autophagy in a transactivation-independent manner. However, the contribution of apoptosis and autophagic cell death to p53-dependent cell death is unclear. Using wild-type (WT) and mutant (MT) p53 inducible cell lines in TP53-null SF126 glioblastoma cells, we examined the apoptosis and autophagic cell death induced by p53. WT p53 expression in SF126 cells induced apoptosis and autophagy, and reduced the cell number. An autophagy inhibitor reduced autophagy, increased the S-phase fraction, and attenuated the inhibition of cell proliferation induced by WT p53. Pan-caspase inhibitor reduced apoptosis but showed weaker inhibition of cell proliferation than the autophagy inhibitor. We concluded that p53-dependent cell death in SF126 cells comprises caspase-dependent and caspase-independent apoptosis and autophagic cell death, and the induction of autophagy as well as apoptosis could be a new strategy to treat some type of WT p53-retaining tumors.

Original languageEnglish
Pages (from-to)799-807
Number of pages9
JournalCancer Science
Issue number4
Publication statusPublished - 2011 Apr


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