Lactate Metabolism in Human Lung Tumors
Open accessAbstract
Cancer cells consume glucose and secrete lactate in culture. It is unknown whether lactate contributes to energy metabolism in living tumors. We previously reported that human non-small-cell lung cancers (NSCLCs) oxidize glucose in the tricarboxylic acid (TCA) cycle. Here, we show that lactate is also a TCA cycle carbon source for NSCLC. In human NSCLC, evidence of lactate utilization was most apparent in tumors with high 18 fluorodeoxyglucose uptake and aggressive oncological behavior. Infusing human NSCLC patients with 13 C-lactate revealed extensive labeling of TCA cycle metabolites. In mice, deleting monocarboxylate transporter-1 (MCT1) from tumor cells eliminated lactate-dependent metabolite labeling, confirming tumor-cell-autonomous lactate uptake. Strikingly, directly comparing lactate and glucose metabolism in vivo indicated that lactate's contribution to the TCA cycle predominates. The data indicate that tumors, including bona fide human NSCLC, can use lactate as a fuel in vivo.
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Monocytes and macrophages are capable of remarkable functional plasticity, displaying diverse phenotypes during wound healing dependent on multiple cues including the environmental niche and the temporal stage of tissue injury and repair.
“Furthermore, monocytes and macrophages are capable of remarkable functional plasticity, displaying diverse phenotypes during wound healing dependent on multiple cues including the environmental niche61,62 and the temporal stage of tissue injury and repair63–66.”
From Fibrosis: from mechanisms to medicines (2020) · cites this paper as [63]
Intravenous infusion of 13C-lactate into human non-small-cell lung cancer patients and mice bearing patient-derived melanomas identified tumors with a propensity for future metastasis, which required MCT1-dependent lactate transport in the mice.
“Intravenous infusion of 13C-lactate into human non-small-cell lung cancer patients and mice bearing patient-derived melanomas identified tumors with a propensity for future metastasis, which required MCT1-dependent lactate transport in the mice (58, 100).”
From Metabolic reprogramming and cancer progression (2020) · cites this paper as [58]
In cultured cells, pyruvate is largely produced from glucose via glycolysis; in vivo, circulating lactate provides an additional major source of tissue pyruvate.
“In cultured cells, pyruvate is largely produced from glucose via glycolysis; in vivo, circulating lactate provides an additional major source of tissue pyruvate (46, 47, 48).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [46]
In most tissues and some tumors, the contribution of circulating lactate to TCA cycle intermediates exceeds that of glucose, supporting the idea that lactate is a fundamental TCA cycle substrate in living organisms.
“In most tissues and some tumors, the contribution of circulating lactate to TCA cycle intermediates exceeds that of glucose, supporting the idea that lactate is a fundamental TCA cycle substrate in living organisms (46, 47).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [46]
Recent studies in vivo have demonstrated that cells import lactate from the circulation via monocarboxylate transporter 1 and subsequently oxidize lactate to form pyruvate, resulting in a large fraction of pyruvate and downstream TCA cycle intermediates being derived from circulating lactate.
“However, recent studies in vivo have demonstrated that cells import lactate from the circulation via monocarboxylate transporter 1 and subsequently oxidize lactate to form pyruvate, resulting in a large fraction of pyruvate and downstream TCA cycle intermediates being derived from circulating lactate (46, 47).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [46]
The contribution of circulating lactate to TCA cycle intermediates exceeds that of glucose in most tissues and tumors.
“As described previously, the contribution of circulating lactate to TCA cycle intermediates exceeds that of glucose in most tissues and tumors (46, 47).”
From Regulation and function of the mammalian tricarboxylic acid cycle (2023) · cites this paper as [46]
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- Authors
- Faubert, B., Li, K. Y., Cai, L., Hensley, C. T., Kim, J., Zacharias, L. G., Yang, C., Do, Q. N., Doucette, S., Burguete, D., Li, H., Huet, G., Yuan, Q., Wigal, T., Butt, Y., Ni, M., Torrealba, J., Oliver, D., Lenkinski, R. E., Malloy, C. R., Wachsmann, J. W., Young, J. D., Kernstine, K., & DeBerardinis, R. J.
- Affiliations
- Children's Medical Center (US)
- The University of Texas Southwestern Medical Center (US)
- Vanderbilt University (US)
- Corresponding author
- DeBerardinis, Ralph J.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 171
- Issue
- 2
- Pages
- 358-371.e9
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5684706
- OpenAlex
- W2763979809
- Cited by
- 1,343
- References
- 41
- Citations by year
- 2026: 135 · 2025: 164 · 2024: 141 · 2023: 160 · 2022: 166 · 2021: 190 · 2020: 158 · 2019: 142 · 2018: 75 · 2017: 9
- FWCI
- 35.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (MFE 140911)
- American Lung Association (RT-306212)
- NIH (R01 DK106348, R35CA220449, P50 CA70907, P41 EB015908, UL1 TR001105)
- Howard Hughes Medical Institute (55108514)
- Welch Foundation (I-1733)
- V Foundation
- UT Southwestern
- NCI Cancer Center (1P30 CA142543-01)
- Philips Healthcare
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cancer and biochemical research
- Keywords
- lactate metabolism, non-small cell lung cancer, TCA cycle, lactate utilization, MCT1, FDG uptake, tumor energy metabolism, tumor glucose metabolism
- MeSH terms
- Monocarboxylate Transport Protein 1, Animals, Blood Chemical Analysis, Carcinoma, Non-Small-Cell Lung, Citric Acid Cycle, Disease Models, Animal, Female, Glyceric Acids, Humans, Lung Neoplasms, Male, Neoplasm Transplantation, Lactic Acid, Monocarboxylic Acid Transporters, Symporters, Cell Line, Tumor, Mice, Heterografts
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