Fundamentals of cancer metabolism

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Abstract

Researchers provide a conceptual framework to understand current knowledge of the fundamentals of cancer metabolism.

Abstract

Tumors reprogram pathways of nutrient acquisition and metabolism to meet the bioenergetic, biosynthetic, and redox demands of malignant cells. These reprogrammed activities are now recognized as hallmarks of cancer, and recent work has uncovered remarkable flexibility in the specific pathways activated by tumor cells to support these key functions. In this perspective, we provide a conceptual framework to understand how and why metabolic reprogramming occurs in tumor cells, and the mechanisms linking altered metabolism to tumorigenesis and metastasis. Understanding these concepts will progressively support the development of new strategies to treat human cancer.

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Most cited references 77

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On the origin of cancer cells.

O WARBURG (1956)

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Bidirectional transport of amino acids regulates mTOR and autophagy.

Paul Nicklin, Philip Bergman, Bailin Zhang … (2009)

Amino acids are required for activation of the mammalian target of rapamycin (mTOR) kinase which regulates protein translation, cell growth, and autophagy. Cell surface transporters that allow amino acids to enter the cell and signal to mTOR are unknown. We show that cellular uptake of L-glutamine and its subsequent rapid efflux in the presence of essential amino acids (EAA) is the rate-limiting step that activates mTOR. L-glutamine uptake is regulated by SLC1A5 and loss of SLC1A5 function inhibits cell growth and activates autophagy. The molecular basis for L-glutamine sensitivity is due to SLC7A5/SLC3A2, a bidirectional transporter that regulates the simultaneous efflux of L-glutamine out of cells and transport of L-leucine/EAA into cells. Certain tumor cell lines with high basal cellular levels of L-glutamine bypass the need for L-glutamine uptake and are primed for mTOR activation. Thus, L-glutamine flux regulates mTOR, translation and autophagy to coordinate cell growth and proliferation.

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Fueling immunity: insights into metabolism and lymphocyte function.

Erika L Pearce, Maya Poffenberger, Chih-Hao Chang … (2013)

Lymphocytes face major metabolic challenges upon activation. They must meet the bioenergetic and biosynthetic demands of increased cell proliferation and also adapt to changing environmental conditions, in which nutrients and oxygen may be limiting. An emerging theme in immunology is that metabolic reprogramming and lymphocyte activation are intricately linked. However, why T cells adopt specific metabolic programs and the impact that these programs have on T cell function and, ultimately, immunological outcome remain unclear. Research on tumor cell metabolism has provided valuable insight into metabolic pathways important for cell proliferation and the influence of metabolites themselves on signal transduction and epigenetic programming. In this Review, we highlight emerging concepts regarding metabolic reprogramming in proliferating cells and discuss their potential impact on T cell fate and function.

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Author and article information

Journal

Journal ID (nlm-ta): Sci Adv

Journal ID (iso-abbrev): Sci Adv

Journal ID (publisher-id): SciAdv

Journal ID (hwp): advances

Title: Science Advances

Publisher: American Association for the Advancement of Science

ISSN (Electronic): 2375-2548

Publication date Collection: May 2016

Publication date (Electronic): 27 May 2016

Volume: 2

Issue: 5

Electronic Location Identifier: e1600200

Affiliations

[1 ]Children’s Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

[2 ]Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.

Author notes

[* ]Corresponding author. Email: Ralph.Deberardinis@ 123456UTSouthwestern.edu (R.J.D.); nav@ 123456northwestern.edu (N.S.C.)

Article

Publisher ID: 1600200

DOI: 10.1126/sciadv.1600200

PMC ID: 4928883

PubMed ID: 27386546

SO-VID: 905b138f-de72-4e26-8109-77c2f4d7cc08

License:

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial license, which permits use, distribution, and reproduction in any medium, so long as the resultant use is not for commercial advantage and provided the original work is properly cited.

History

Date received : 01 February 2016

Date accepted : 29 April 2016

Funding

Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;

Award ID: ID0E1EAG7327

Award ID: R01 CA123067

Award Recipient : Navdeep Chandel

Funded by: FundRef http://dx.doi.org/10.13039/100000054, National Cancer Institute;

Award ID: ID0EAMAG7328

Award ID: 5R01CA157996

Award Recipient : Ralph DeBerardinis

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Copyeditor Mikee Bernabe

Keywords: cancer,metabolism,mitochondria,glycolysis,ros,oncogenes

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Keywords: cancer, metabolism, mitochondria, glycolysis, ros, oncogenes

Fundamentals of cancer metabolism

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Abstract

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Cancer Metabolism

Most cited references 77

On the origin of cancer cells.

Bidirectional transport of amino acids regulates mTOR and autophagy.

Fueling immunity: insights into metabolism and lymphocyte function.

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