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      Cancer metabolic reprogramming: importance, main features, and potentials for precise targeted anti-cancer therapies

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          Abstract

          Cancer cells are well documented to rewire their metabolism and energy production networks to support and enable rapid proliferation, continuous growth, survival in harsh conditions, invasion, metastasis, and resistance to cancer treatments. Since Dr. Otto Warburg’s discovery about altered cancer cell metabolism in 1930, thousands of studies have shed light on various aspects of cancer metabolism with a common goal to find new ways for effectively eliminating tumor cells by targeting their energy metabolism. This review highlights the importance of the main features of cancer metabolism, summarizes recent remarkable advances in this field, and points out the potentials to translate these scientific findings into life-saving diagnosis and therapies to help cancer patients.

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          On the origin of cancer cells.

          O WARBURG (1956)
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            TIGAR, a p53-Inducible Regulator of Glycolysis and Apoptosis

            Karim Bensaad, Atsushi Tsuruta, Mary A. Selak … (2006)
            The p53 tumor-suppressor protein prevents cancer development through various mechanisms, including the induction of cell-cycle arrest, apoptosis, and the maintenance of genome stability. We have identified a p53-inducible gene named TIGAR (TP53-induced glycolysis and apoptosis regulator). TIGAR expression lowered fructose-2,6-bisphosphate levels in cells, resulting in an inhibition of glycolysis and an overall decrease in intracellular reactive oxygen species (ROS) levels. These functions of TIGAR correlated with an ability to protect cells from ROS-associated apoptosis, and consequently, knockdown of endogenous TIGAR expression sensitized cells to p53-induced death. Expression of TIGAR may therefore modulate the apoptotic response to p53, allowing survival in the face of mild or transient stress signals that may be reversed or repaired. The decrease of intracellular ROS levels in response to TIGAR may also play a role in the ability of p53 to protect from the accumulation of genomic damage.
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              AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy.

              D Hardie (2007)
              The SNF1/AMP-activated protein kinase (AMPK) family maintains the balance between ATP production and consumption in all eukaryotic cells. The kinases are heterotrimers that comprise a catalytic subunit and regulatory subunits that sense cellular energy levels. When energy status is compromised, the system activates catabolic pathways and switches off protein, carbohydrate and lipid biosynthesis, as well as cell growth and proliferation. Surprisingly, recent results indicate that the AMPK system is also important in functions that go beyond the regulation of energy homeostasis, such as the maintenance of cell polarity in epithelial cells.
              Article 0 comments Cited 635 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Biol Med
                Journal ID (iso-abbrev): Cancer Biol Med
                Journal ID (publisher-id): CBM
                Title: Cancer Biology & Medicine
                Publisher: Chinese Anti-Cancer Association
                ISSN (Print): 2095-3941
                Publication date (Print and electronic): March 2014
                Publication date (Print): March 2014
                Volume: 11
                Issue: 1
                Pages: 1-19
                Affiliations
                Department of Molecular and Cellular Oncology, Department of General Internal Medicine, Ambulatory Treatment and Emergency Care, Department of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, 1515 Holcombe Blvd, Houston, Texas, TX77030, USA
                Author notes

                Correspondence to: Sai-Ching Jim Yeung; Mong-Hong Lee

                E-mail: syeung@ 123456mdanderson.org ; mhlee@ 123456mdanderson.org

                Article
                Publisher ID: cbm-11-01-001
                DOI: 10.7497/j.issn.2095-3941.2014.01.001
                PMC ID: 3969803
                PubMed ID: 24738035
                SO-VID: e473908f-d00a-487d-9f3d-e3d1bce48389
                Copyright © 2014 Cancer Biology & Medicine
                License:

                This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/

                History
                Date received : 06 November 2013
                Date accepted : 19 January 2014
                Categories
                Subject: Review

                Keywords: cell cycle,energy metabolism,glycolysis,glutaminolysis,mitochondria biogenesis
                Data availability:
                Keywords: cell cycle, energy metabolism, glycolysis, glutaminolysis, mitochondria biogenesis

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