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Cytosolic FoxO1 is essential for the induction of autophagy and tumour suppressor activity
Ying Zhao1, Jing Yang1, Wenjuan Liao1, Xiangyu Liu1, Hui Zhang1,2, Shan Wang2, Donglai Wang1, Jingnan Feng1, Li Yu3 & Wei-Guo Zhu1,4
Autophagy is characterized by the sequestration of bulk cytoplasm, including damaged proteins and organelles, and delivery of the cargo to lysosomes for degradation. Although the autophagic pathway is also linked to tumour suppression activity, the mechanism is not yet clear. Here we report that cytosolic FoxO1, a forkhead O family protein, is a mediator of autophagy. Endogenous FoxO1 was required for autophagy in human cancer cell lines in response to oxidative stress or serum starvation, but this process was independent of the transcriptional activity of FoxO1. In response to stress, FoxO1 was acetylated by dissociation from sirtuin-2 (SIRT2), a NAD+-dependent histone deacetylase, and the acetylated FoxO1 bound to Atg7, an E1-like protein, to influence the autophagic process leading to cell death. This FoxO1-modulated cell death is associated with tumour suppressor activity in human colon tumours and a xenograft mouse model. Our finding links the anti-neoplastic activity of FoxO1 and the process of autophagy.
1 Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100191, China.
2 Department of Surgery, the Secondary Affiliated Hospital, Peking University Health Science Center, Beijing 100044, China.
3 Department of Biological Science and Biotechnology, Tsinghua University, Beijing 100084, China.
4 School of Oncology, Peking University Health Science Center, Beijing 00142, China.
