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      The role of Wnt signaling pathway in tumor metabolic reprogramming

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          Abstract

          The occurrence and development of tumors is a complex process involving long-term multi-factor participation. In this process, tumor cells from a set of abnormal metabolic patterns that are different from normal cells. This abnormal metabolic change is called metabolic reprogramming of tumors. Wnt signaling pathway is one of the critical signaling pathways regulating cell proliferation and differentiation. In recent years, it has been found that Wnt signaling participates in the occurrence and development of malignant tumors by affecting metabolic reprogramming. This paper reviews the role of Wnt signaling in tumor metabolic reprogramming to provide crucial theoretical guidance for targeted therapy and drug response of tumors.

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          On the origin of cancer cells.

          O WARBURG (1956)
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            The return of metabolism: biochemistry and physiology of the pentose phosphate pathway

            Anna Stincone, Alessandro Prigione, Thorsten Cramer … (2014)
            The pentose phosphate pathway (PPP) is a fundamental component of cellular metabolism. The PPP is important to maintain carbon homoeostasis, to provide precursors for nucleotide and amino acid biosynthesis, to provide reducing molecules for anabolism, and to defeat oxidative stress. The PPP shares reactions with the Entner–Doudoroff pathway and Calvin cycle and divides into an oxidative and non-oxidative branch. The oxidative branch is highly active in most eukaryotes and converts glucose 6-phosphate into carbon dioxide, ribulose 5-phosphate and NADPH. The latter function is critical to maintain redox balance under stress situations, when cells proliferate rapidly, in ageing, and for the ‘Warburg effect’ of cancer cells. The non-oxidative branch instead is virtually ubiquitous, and metabolizes the glycolytic intermediates fructose 6-phosphate and glyceraldehyde 3-phosphate as well as sedoheptulose sugars, yielding ribose 5-phosphate for the synthesis of nucleic acids and sugar phosphate precursors for the synthesis of amino acids. Whereas the oxidative PPP is considered unidirectional, the non-oxidative branch can supply glycolysis with intermediates derived from ribose 5-phosphate and vice versa, depending on the biochemical demand. These functions require dynamic regulation of the PPP pathway that is achieved through hierarchical interactions between transcriptome, proteome and metabolome. Consequently, the biochemistry and regulation of this pathway, while still unresolved in many cases, are archetypal for the dynamics of the metabolic network of the cell. In this comprehensive article we review seminal work that led to the discovery and description of the pathway that date back now for 80 years, and address recent results about genetic and metabolic mechanisms that regulate its activity. These biochemical principles are discussed in the context of PPP deficiencies causing metabolic disease and the role of this pathway in biotechnology, bacterial and parasite infections, neurons, stem cell potency and cancer metabolism.
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              FAT SIGNALS - Lipases and Lipolysis in Lipid Metabolism and Signaling

              Rudolf Zechner, Robert Zimmermann, Thomas O. Eichmann … (2012)
              Lipolysis is defined as the catabolism of triacylglycerols stored in cellular lipid droplets. Recent discoveries of essential lipolytic enzymes and characterization of numerous regulatory proteins and mechanisms have fundamentally changed our perception of lipolysis and its impact on cellular metabolism. New findings that lipolytic products and intermediates participate in cellular signaling processes and that “lipolytic signaling” is particularly important in many nonadipose tissues unveil a previously underappreciated aspect of lipolysis, which may be relevant for human disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Cancer
                Journal ID (iso-abbrev): J Cancer
                Journal ID (publisher-id): jca
                Title: Journal of Cancer
                Publisher: Ivyspring International Publisher (Sydney )
                ISSN (Electronic): 1837-9664
                Publication date Collection: 2019
                Publication date (Electronic): 9 June 2019
                Volume: 10
                Issue: 16
                Pages: 3789-3797
                Affiliations
                [1 ]NHC Key Laboratory of Carcinogenesis, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, Hunan 410078, China
                [2 ]The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Science, Central South University, Changsha 410078, China
                [3 ]Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China.
                [4 ]Department of Cancer Biology, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio 44195, USA
                Author notes

                # These authors contributed equally.

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                Publisher ID: jcav10p3789
                DOI: 10.7150/jca.31166
                PMC ID: 6636296
                PubMed ID: 31333796
                SO-VID: 726341f6-59ec-41c6-b960-b49b14081fff
                Copyright © © Ivyspring International Publisher
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license ( https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                Date received : 2 November 2018
                Date accepted : 29 May 2019
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: tumor metabolic reprogramming,wnt signaling,targeted therapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: tumor metabolic reprogramming, wnt signaling, targeted therapy

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