NDLI: The metabolic demands of cancer cells are coupled to their size and protein synthesis rates

Content Provider	Springer Nature : BioMed Central
Author	Dolfi, Sonia C Chan, Leo Li-Ying Qiu, Jean Tedeschi, Philip M Bertino, Joseph R Hirshfield, Kim M Oltvai, Zoltán N Vazquez, Alexei
Abstract	Background Although cells require nutrients to proliferate, most nutrient exchange rates of the NCI60 panel of cancer cell lines correlate poorly with their proliferation rate. Here, we provide evidence indicating that this inconsistency is rooted in the variability of cell size. Results We integrate previously reported data characterizing genome copy number variations, gene expression, protein expression and exchange fluxes with our own measurements of cell size and protein content in the NCI60 panel of cell lines. We show that protein content, DNA content, and protein synthesis per cell are proportional to the cell volume, and that larger cells proliferate slower than smaller cells. We estimate the metabolic fluxes of these cell lines and show that their magnitudes are proportional to their protein synthesis rate and, after correcting for cell volume, to their proliferation rate. At the level of gene expression, we observe that genes expressed at higher levels in smaller cells are enriched for genes involved in cell cycle, while genes expressed at higher levels in large cells are enriched for genes expressed in mesenchymal cells. The latter finding is further corroborated by the induction of those same genes following treatment with TGFβ, and the high vimentin but low E-cadherin protein levels in the larger cells. We also find that aromatase inhibitors, statins and mTOR inhibitors preferentially inhibit the in vitro growth of cancer cells with high protein synthesis rates per cell. Conclusions The NCI60 cell lines display various metabolic activities, and the type of metabolic activity that they possess correlates with their cell volume and protein content. In addition to cell proliferation, cell volume and/or biomarkers of protein synthesis may predict response to drugs targeting cancer metabolism.
Related Links	https://cancerandmetabolism.biomedcentral.com/counter/pdf/10.1186/2049-3002-1-20.pdf
Ending Page	13
Page Count	13
Starting Page	1
File Format	HTM / HTML
ISSN	20493002
DOI	10.1186/2049-3002-1-20
Journal	Cancer & Metabolism
Issue Number	1
Volume Number	1
Language	English
Publisher	BioMed Central
Publisher Date	2013-11-07
Access Restriction	Open
Subject Keyword	Cancer Research Oncology Metabolomics Metabolic Diseases Imaging Radiology Cell Biology Cancer metabolism Cell size Proliferation rate Mesenchymal cells Cholesterol synthesis inhibitors
Content Type	Text
Resource Type	Article
Subject	Cancer Research
Journal Impact Factor	6/2023
5-Year Journal Impact Factor	5.4/2023

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1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
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3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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The metabolic demands of cancer cells are coupled to their size and protein synthesis rates

Correction: Cholesterol reprograms glucose and lipid metabolism to promote proliferation in colon cancer cells

Cholesterol reprograms glucose and lipid metabolism to promote proliferation in colon cancer cells

Metabolic requirements for cancer cell proliferation

Prostate cancer cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover

Protein synthesis inhibitors stimulate MondoA transcriptional activity by driving an accumulation of glucose 6-phosphate

Mesenchymal phenotype predisposes lung cancer cells to impaired proliferation and redox stress in response to glutaminase inhibition

Cell proliferation and tissue remodeling are major determinants of cancer metabolism and the response to drugs targeting metabolism

Cancer & Metabolism

The metabolic demands of cancer cells are coupled to their size and protein synthesis rates

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The metabolic demands of cancer cells are coupled to their size and protein synthesis rates

Correction: Cholesterol reprograms glucose and lipid metabolism to promote proliferation in colon cancer cells

Cholesterol reprograms glucose and lipid metabolism to promote proliferation in colon cancer cells

Metabolic requirements for cancer cell proliferation

Prostate cancer cell proliferation is influenced by LDL-cholesterol availability and cholesteryl ester turnover

Protein synthesis inhibitors stimulate MondoA transcriptional activity by driving an accumulation of glucose 6-phosphate

Mesenchymal phenotype predisposes lung cancer cells to impaired proliferation and redox stress in response to glutaminase inhibition

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Cancer & Metabolism

The metabolic demands of cancer cells are coupled to their size and protein synthesis rates