期刊
CELL REPORTS
卷 20, 期 7, 页码 1692-1704出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.07.055
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资金
- USNIH [R01GM115366, R01CA160417, R01CA181450]
- Natural Science Foundation of Guangdong Province [2016A030308011]
- American Cancer Society [RSG-16-014-01-CDD]
- National Natural Science Foundation of China [31671435, 81400132, 8177100253]
- National Funds of Developing Local Colleges and Universities Grant [B16056001]
- Frontier and Key Technology Innovation Special Grant from the Department of Science and Technology of Guangdong Province [2016B030229008]
- Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme
- University of Pittsburgh Cancer Institute [P30CA047904]
- Ligue contre le Cancer (equipe labelisee)
- Agence National de la Recherche (ANR) Projets blancs
- ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases
- Association pour la recherche sur le cancer (ARC)
- Canceropole Ile-de-France
- Institut National du Cancer (INCa)
- Institut Universitaire de France
- Fondation pour la Recherche Medicale (FRM)
- European Commission (ArtForce)
- European Research Council (ERC)
- LeDucq Foundation
- LabEx Immuno-Oncology
- RHU Torino Lumiere
- SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE)
- SIRIC Cancer Research and Personalized Medicine (CARPEM)
- Paris Alliance of Cancer Research Institutes (PACRI)
Ferroptosis is a form of regulated cell death that may facilitate the selective elimination of tumor cells. The tumor suppressor p53 (TP53) has been demonstrated to promote ferroptosis via a transcriptiondependent mechanism. Here, we show that TP53 limits erastin-induced ferroptosis by blocking dipeptidyl-peptidase-4 (DPP4) activity in a transcription-independent manner. Loss of TP53 prevents nuclear accumulation of DPP4 and thus facilitates plasma-membrane-associated DPP4-dependent lipid peroxidation, which finally results in ferroptosis. These findings reveal a direct molecular link between TP53 and DPP4 in the control of lipid metabolism and may provide a precision medicine strategy for the treatment of colorectal cancer by induction of ferroptosis.
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