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Lactate Metabolism in Human Lung Tumors
Brandon Faubert1, Kevin Y Li1, Ling Cai2
1Children's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Cell
|October 7, 2017
Summary
Tumors, including non-small cell lung cancer (NSCLC), can utilize lactate as an energy source. This study reveals lactate is a primary fuel for the tricarboxylic acid (TCA) cycle in NSCLC.
Area of Science:
- Oncology
- Cancer Metabolism
- Biochemistry
Background:
- Cancer cells metabolize glucose, secreting lactate.
- The role of lactate in the energy metabolism of living tumors remains unclear.
- Previous work showed human non-small cell lung cancers (NSCLCs) utilize glucose in the tricarboxylic acid (TCA) cycle.
Purpose of the Study:
- To investigate if lactate serves as a carbon source for the TCA cycle in NSCLC.
- To determine the extent of lactate utilization in human NSCLC in vivo.
- To compare the contribution of lactate versus glucose to tumor metabolism.
Main Methods:
- Infusion of 13C-lactate into human NSCLC patients.
- Analysis of TCA cycle metabolite labeling.
- Genetic deletion of monocarboxylate transporter-1 (MCT1) in mouse tumor models.
- In vivo metabolic flux analysis comparing lactate and glucose.
Main Results:
- Lactate was identified as a significant carbon source for the TCA cycle in human NSCLC.
- Lactate utilization was more pronounced in tumors with high 18-fluorodeoxyglucose uptake and aggressive behavior.
- Tumor-cell-autonomous lactate uptake was confirmed by MCT1 deletion in mice.
- In vivo, lactate's contribution to the TCA cycle was found to be predominant over glucose.
Conclusions:
- Human NSCLC and other tumors can utilize lactate as a fuel source in vivo.
- Lactate plays a critical role in the metabolic reprogramming of cancer cells.
- Targeting lactate metabolism presents a potential therapeutic strategy for NSCLC.
