Journal
NATURE CELL BIOLOGY
Volume 20, Issue 5, Pages 597-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41556-018-0083-6
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Funding
- National Institutes of Health (NIH)/National Cancer Institute (NCI) [R01CA218140, R01CA166020, R01CA206911, R01CA163586]
- California Breast Cancer Research Program [20IB-0118]
- Breast Cancer Research Foundation-AACR grant [12-60-26-WANG]
- National Key Technology R&D Program of China [2015BAI12B12]
- NIH/NCI [P30CA23100, P30CA33572]
- NATIONAL CANCER INSTITUTE [P30CA033572, R01CA163586, R01CA212119, P30CA023100, R01CA166020, R01CA206911, R01CA218140] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM086171] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [S10OD018164] Funding Source: NIH RePORTER
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Cancer and other cells residing in the same niche engage various modes of interactions to synchronize and buffer the negative effects of environmental changes. Extracellular microRNAs (miRNAs) have recently been implicated in the intercellular crosstalk. Here we show a mechanistic model involving breast-cancer-secreted, extracellular-vesicle-encapsulated miR-105, which is induced by the oncoprotein MYC in cancer cells and, in turn, activates MYC signalling in cancer-associated fibroblasts (CAFs) to induce a metabolic program. This results in the capacity of CAFs to display different metabolic features in response to changes in the metabolic environment. When nutrients are sufficient, miR-105-reprogrammed CAFs enhance glucose and glutamine metabolism to fuel adjacent cancer cells. When nutrient levels are low and metabolic by-products accumulate, these CAFs detoxify metabolic wastes, including lactic acid and ammonium, by converting them into energy-rich metabolites. Thus, the miR-105-mediated metabolic reprogramming of stromal cells contributes to sustained tumour growth by conditioning the shared metabolic environment.
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