Abstract:
:Although Beclin 1 and mTOR are considered to be the main molecules to modulate the autophagic process, searching for other autophagy-regulating molecules is still an ongoing challenge to scientists. Here we demonstrated that FoxO1, a forkhead O family protein, is a mediator of autophagy. Upon oxidative stress or serum starvation, endogenous FoxO1 was required for autophagy in human cancer cell lines, and this process was independent of FoxO1's transcriptional activity as well as mTOR or Beclin 1. In response to stress, FoxO1 dissociated from an NAD(+)-dependent histone deacetylase SIRT2 and FoxO1 thus became acetylated and in turn bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death. In particular, cytosolic FoxO1 suppressed tumor xenograft growth in nude mice in an autophagy-dependent manner. Our studies provide evidence that cytosolic FoxO1-induced autophagy is associated with tumor suppression function.
journal_name
Autophagyjournal_title
Autophagyauthors
Zhao Y,Wang L,Yang J,Zhang P,Ma K,Zhou J,Liao W,Zhu WGdoi
10.4161/auto.6.7.13289subject
Has Abstractpub_date
2010-10-01 00:00:00pages
988-90issue
7eissn
1554-8627issn
1554-8635pii
13289journal_volume
6pub_type
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