Journal
CELL METABOLISM
Volume 27, Issue 6, Pages 1249-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2018.04.003
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Funding
- NIH [R21CA201963, R35GM122465, U01 CA214300]
- NSF [1511357, 1350659]
- National Natural Science Foundation of China [31771513]
- Strategic Priority Research Program of the Chinese Academy of Sciences [XDPB03]
- CAS Pioneer Hundred Talents Program
- Thousand Young Talents Program of China
- Directorate For Engineering
- Div Of Chem, Bioeng, Env, & Transp Sys [1350659] Funding Source: National Science Foundation
- Div Of Chem, Bioeng, Env, & Transp Sys
- Directorate For Engineering [1511357] Funding Source: National Science Foundation
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Cancer metastasis accounts for the majority of cancer-related deaths and remains a clinical challenge. Metastatic cancer cells generally resemble cells of the primary cancer, but they may be influenced by the milieu of the organs they colonize. Here, we show that colorectal cancer cells undergo metabolic reprogramming after they metastasize and colonize the liver, a key metabolic organ. In particular, via GATA6, metastatic cells in the liver upregulate the enzyme aldolase B (ALDOB), which enhances fructose metabolism and provides fuel for major pathways of central carbon metabolism during tumor cell proliferation. Targeting ALDOB or reducing dietary fructose significantly reduces liver metastatic growth but has little effect on the primary tumor. Our findings suggest that metastatic cells can take advantage of reprogrammed metabolism in their new microenvironment, especially in a metabolically active organ such as the liver. Manipulation of involved pathways may affect the course of metastatic growth.
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