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      Reprogramming glucose metabolism in cancer: can it be exploited for cancer therapy?

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      Journal: Nature Reviews Cancer
      Publisher: Springer Science and Business Media LLC

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          Abstract

          In recent years there has been a growing interest among cancer biologists in cancer metabolism. This Review summarizes past and recent advances in our understanding of the reprogramming of glucose metabolism in cancer cells, which is mediated by oncogenic drivers and by the undifferentiated character of cancer cells. The reprogrammed glucose metabolism in cancer cells is required to fulfil anabolic demands. This Review discusses the possibility of exploiting the reprogrammed glucose metabolism for therapeutic approaches that selectively target cancer cells.

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          Targeting lactate metabolism for cancer therapeutics.

          Joanne R. Doherty, John L. Cleveland (2013)
          Lactate, once considered a waste product of glycolysis, has emerged as a critical regulator of cancer development, maintenance, and metastasis. Indeed, tumor lactate levels correlate with increased metastasis, tumor recurrence, and poor outcome. Lactate mediates cancer cell intrinsic effects on metabolism and has additional non-tumor cell autonomous effects that drive tumorigenesis. Tumor cells can metabolize lactate as an energy source and shuttle lactate to neighboring cancer cells, adjacent stroma, and vascular endothelial cells, which induces metabolic reprogramming. Lactate also plays roles in promoting tumor inflammation and in functioning as a signaling molecule that stimulates tumor angiogenesis. Here we review the mechanisms of lactate production and transport and highlight emerging evidence indicating that targeting lactate metabolism is a promising approach for cancer therapeutics.
          Article 0 comments Cited 469 times – based on 0 reviews     Review now
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            The SLC2 (GLUT) family of membrane transporters.

            Mike Mueckler, Bernard Thorens (2013)
            GLUT proteins are encoded by the SLC2 genes and are members of the major facilitator superfamily of membrane transporters. Fourteen GLUT proteins are expressed in the human and they are categorized into three classes based on sequence similarity. All GLUTs appear to transport hexoses or polyols when expressed ectopically, but the primary physiological substrates for several of the GLUTs remain uncertain. GLUTs 1-5 are the most thoroughly studied and all have well established roles as glucose and/or fructose transporters in various tissues and cell types. The GLUT proteins are comprised of ∼500 amino acid residues, possess a single N-linked oligosaccharide, and have 12 membrane-spanning domains. In this review we briefly describe the major characteristics of the 14 GLUT family members. Copyright © 2012 Elsevier Ltd. All rights reserved.
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              Lactate: a metabolic key player in cancer.

              Franziska Hirschhaeuser, Ulrike G A Sattler, Wolfgang Mueller-Klieser (2011)
              Increased glucose uptake and accumulation of lactate, even under normoxic conditions (i.e., aerobic glycolysis or the Warburg Effect), is a common feature of cancer cells. This phenomenon clearly indicates that lactate is not a surrogate of tumor hypoxia. Tumor lactate can predict for metastases and overall survival of patients, as shown by several studies of different entities. Metastasis of tumors is promoted by lactate-induced secretion of hyaluronan by tumor-associated fibroblasts that create a milieu favorable for migration. Lactate itself has been found to induce the migration of cells and cell clusters. Furthermore, radioresistance has been positively correlated with lactate concentrations, suggesting an antioxidative capacity of lactate. Findings on interactions of tumor metabolites with immune cells indicate a contribution of lactate to the immune escape. Furthermore, lactate bridges the gap between high lactate levels in wound healing, chronic inflammation, and cancer development. Tumor cells ensure sufficient oxygen and nutrient supply for proliferation through lactate-induced secretion of VEGF, resulting in the formation of new vessels. In summary, accumulation of lactate in solid tumors is a pivotal and early event in the development of malignancies. The determination of lactate should enter further clinical trials to confirm its relevance in cancer biology. ©2011 AACR
              Article 0 comments Cited 449 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Title: Nature Reviews Cancer
                Abbreviated Title: Nat Rev Cancer
                Publisher: Springer Science and Business Media LLC
                ISSN (Print): 1474-175X
                ISSN (Electronic): 1474-1768
                Publication date Created: October 2016
                Publication date (Electronic): September 16 2016
                Publication date (Print): October 2016
                Volume: 16
                Issue: 10
                Pages: 635-649
                Article
                DOI: 10.1038/nrc.2016.77
                PMC ID: 5516800
                PubMed ID: 27634447
                SO-VID: 273195ce-32b2-48cc-a89a-1ba989eb6376
                Copyright © © 2016
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                http://www.springer.com/tdm

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