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Glucose Deprivation Contributes to the Development of KRAS Pathway Mutations in Tumor Cells

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Yun, Jihye, Rago, Carlo, Cheong, Ian, Pagliarini, Ray, Angenendt, Philipp, Rajagopalan, Harith, Schmidt, Kerstin, Willson, James K. V., Markowitz, Sandy, Zhou, Shibin, Diaz, Luis A., Velculescu, Victor E., Lengauer, Christoph, Kinzler, Kenneth W., Vogelstein, Bert, Papadopoulos, Nickolas·2009·Science

DOI 10.1126/science.1174229PMC PMC2820374

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Abstract

Desperately Seeking Glucose: Mutations in oncogenes and tumor suppressor genes allow cancer cells to outgrow their neighboring healthy cells. What microenvironmental conditions provide a selective growth advantage to these cells? Yun et al. (p. 1555 , published online 6 August) identify low glucose availability as a microenvironmental factor driving the acquisition of KRAS oncogenic mutations that allow cancer cells to survive and grow. In genetically matched colorectal cancer cells that differed only in the mutational status of the KRAS oncogene, mutant cells selectively overexpressed glucose transporter-1 and exhibited enhanced glucose uptake and glycolysis. When cells with wild-type KRAS were placed in a low-glucose environment, very few cells survived but most of the survivors expressed high levels of glucose transporter-1, and a small percentage of the survivors had acquired new KRAS mutations. Thus, glucose deprivation may help to drive the acquisition of cell growth–promoting oncogenic mutations during tumor development.

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Authors: Yun, J., Rago, C., Cheong, I., Pagliarini, R., Angenendt, P., Rajagopalan, H., Schmidt, K., Willson, J. K. V., Markowitz, S., Zhou, S., Diaz, L. A., Velculescu, V. E., Lengauer, C., Kinzler, K. W., Vogelstein, B., & Papadopoulos, N.
Affiliations: Howard Hughes Medical Institute (US)
The Ludwig Center for Cancer Genetics and Therapeutics and The Howard Hughes Medical Institute at the Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.
Harold C. Simmons Comprehensive Cancer Center (US)
Corresponding author: Rajagopalan, Harith
Vogelstein, Bert
ORCID: Yun, Jihye
Cheong, Ian
Rajagopalan, Harith
Willson, James K. V.
Zhou, Shibin
Diaz, Luis A.
Velculescu, Victor E.
Kinzler, Kenneth W.
Vogelstein, Bert
Papadopoulos, Nickolas
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 2009-09-18
Volume: 325
Issue: 5947
Pages: 1555-1559
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.1174229
PMC: PMC2820374
OpenAlex: W1970766774
Cited by: 914
References: 42
Citations by year: 2026: 21 · 2025: 39 · 2024: 43 · 2023: 47 · 2022: 48 · 2021: 60 · 2020: 70 · 2019: 75 · 2018: 61 · 2017: 60 · 2016: 63 · 2015: 51 · 2014: 87 · 2013: 48 · 2012: 61
FWCI: 15.77
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Science (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (CA43460, R37CA043460, P50CA062924, CA 62924)
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 › Cancer Research › Cancer Genomics and Diagnostics
Keywords: glucose deprivation, KRAS mutation, BRAF mutation, GLUT1, glucose transporter 1, colorectal cancer cell lines, tumor progression, glycolysis, glucose uptake, 3-bromopyruvate, transcriptome
MeSH terms: Animals, Glucose, Glycolysis, Humans, Mice, Nude, Mutation, Neoplasm Transplantation, Pyruvates, Genes, ras, Transplantation, Heterologous, Colorectal Neoplasms, Gene Expression Regulation, Neoplastic, Gene Targeting, Lactic Acid, Oligonucleotide Array Sequence Analysis, Cell Line, Tumor, Proto-Oncogene Proteins B-raf, Cell Proliferation, Glucose Transporter Type 1, Mice

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Glucose Deprivation Contributes to the Development of KRAS Pathway Mutations in Tumor Cells

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