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Cited by 351

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Tumor metabolism: cancer cells give and take lactate

Open access
Semenza, Gregg L.·2008·Journal of Clinical Investigation

Abstract

Tumors contain well-oxygenated (aerobic) and poorly oxygenated (hypoxic) regions, which were thought to utilize glucose for oxidative and glycolytic metabolism, respectively. In this issue of the JCI, Sonveaux et al. show that human cancer cells cultured under hypoxic conditions convert glucose to lactate and extrude it, whereas aerobic cancer cells take up lactate via monocarboxylate transporter 1 (MCT1) and utilize it for oxidative phosphorylation (see the related article beginning on page 3930). When MCT1 is inhibited, aerobic cancer cells take up glucose rather than lactate, and hypoxic cancer cells die due to glucose deprivation. Treatment of tumor-bearing mice with an inhibitor of MCT1 retarded tumor growth. MCT1 expression was detected exclusively in nonhypoxic regions of human cancer biopsy samples, and in combination, these data suggest that MCT1 inhibition holds potential as a novel cancer therapy.

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Crossref · 10.1172/jci37373

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Metadata

Authors
Semenza, G. L.
Venue
Journal of Clinical Investigation
Published
2008-11-20
Volume
118
Issue
12
Pages
3835-7
ISSN
0021-9738 (ISSN-L)
OpenAlex
W1986119405
Cited by
351
References
2
FWCI
5.36
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Tumor metabolism: cancer cells give and take lactate. https://app.cochat.ai/papers/10.1172/jci37373
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Semenza, G. L. (2008). Tumor metabolism: cancer cells give and take lactate. Journal of Clinical Investigation. https://doi.org/10.1172/jci37373

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.