Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms15503
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Funding
- UT Dallas start-up fund
- American Lung Association [LCD-400239]
- NIH [R01 CA163649, K25 AR063761]
- SPORE [2P50 CA127207]
- Project for Development of Innovative Research on Cancer Therapeutics
- Japan Agency for Medical Research and Development
- JSPS [JP26111005]
- Takeda Science Foundation [JP25461937]
- JST PRESTO [16K09493, 26111003]
- Banyu Life Science Foundation International
- Takeda Science Foundation
- Welch Foundation [AT-1595]
- NCI [P50CA70907]
- Cancer Prevention and Research Institute of Texas (CPRIT) [RP110708]
- Grants-in-Aid for Scientific Research [16K09493, 15K21759, 26111003, 26111005] Funding Source: KAKEN
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Adenocarcinoma (ADC) and squamous cell carcinoma (SqCC) are the two predominant subtypes of non-small cell lung cancer (NSCLC) and are distinct in their histological, molecular and clinical presentation. However, metabolic signatures specific to individual NSCLC subtypes remain unknown. Here, we perform an integrative analysis of human NSCLC tumour samples, patient-derived xenografts, murine model of NSCLC, NSCLC cell lines and The Cancer Genome Atlas (TCGA) and reveal a markedly elevated expression of the GLUT1 glucose transporter in lung SqCC, which augments glucose uptake and glycolytic flux. We show that a critical reliance on glycolysis renders lung SqCC vulnerable to glycolytic inhibition, while lung ADC exhibits significant glucose independence. Clinically, elevated GLUT1-mediated glycolysis in lung SqCC strongly correlates with high F-18-FDG uptake and poor prognosis. This previously undescribed metabolic heterogeneity of NSCLC subtypes implicates significant potential for the development of diagnostic, prognostic and targeted therapeutic strategies for lung SqCC, a cancer for which existing therapeutic options are clinically insufficient.
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