期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms16031
关键词
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资金
- National Institute of Cancer [INCa PLBIO15-217]
- SIRIC INCa-Inserm-DGOS [6038]
- Plan Cancer [C13056AS]
- Fondation de France
- French Ministry for Research and Education (MENRT)
- Chief Scientist Office [ETM/374]
- 'Ligue contre le cancer'
- Canceropole PACA
- Inserm Plan Cancer [C13056AS]
- Lustgarten Foundation
- Ludwig Center at MIT [SU2C, P30CA14051]
- Howard Hughes Medical Institute (Faculty Scholars Award)
- [F30 CA183474]
- [T32GM007753]
- [INCaPLBIO15-217]
- Chief Scientist Office [ETM/374] Funding Source: researchfish
Tissue architecture contributes to pancreatic ductal adenocarcinoma (PDAC) phenotypes. Cancer cells within PDAC form gland-like structures embedded in a collagen-rich meshwork where nutrients and oxygen are scarce. Altered metabolism is needed for tumour cells to survive in this environment, but the metabolic modifications that allow PDAC cells to endure these conditions are incompletely understood. Here we demonstrate that collagen serves as a proline reservoir for PDAC cells to use as a nutrient source when other fuels are limited. We show PDAC cells are able to take up collagen fragments, which can promote PDAC cell survival under nutrient limited conditions, and that collagen-derived proline contributes to PDAC cell metabolism. Finally, we show that proline oxidase (PRODH1) is required for PDAC cell proliferation in vitro and in vivo. Collectively, our results indicate that PDAC extracellular matrix represents a nutrient reservoir for tumour cells highlighting the metabolic flexibility of this cancer.
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