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      Regulatory Mechanisms of LncRNAs in Cancer Glycolysis: Facts and Perspectives

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          Abstract

          Cancer cells exhibit distinct metabolic characteristics that employ glycolysis to provide energy and intermediary metabolites. This aberrant metabolic phenotype favors cancer progression. LncRNAs are transcripts longer than 200 nucleotides that do not encode proteins. LncRNAs contribute to cancer progression and therapeutic resistance and affect aerobic glycolysis via multiple mechanisms, including modulating glycolytic transporters and enzymes. Further, dysregulated signaling pathways are vital for glycolysis. In this review, we highlight regulatory mechanisms for lncRNAs in aerobic glycolysis that provide novel insights into cancer development. Moreover, a comprehensive understanding of the regulatory mechanisms of lncRNAs in aerobic glycolysis can provide new strategies for clinical cancer management.

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          Hallmarks of Cancer: The Next Generation

          Douglas Hanahan, Robert A. Weinberg (2011)
          The hallmarks of cancer comprise six biological capabilities acquired during the multistep development of human tumors. The hallmarks constitute an organizing principle for rationalizing the complexities of neoplastic disease. They include sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. Underlying these hallmarks are genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions. Conceptual progress in the last decade has added two emerging hallmarks of potential generality to this list-reprogramming of energy metabolism and evading immune destruction. In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the "tumor microenvironment." Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Understanding the Warburg effect: the metabolic requirements of cell proliferation.

            Matthew G Vander Heiden, Lewis C Cantley, Craig B Thompson (2009)
            In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative phosphorylation to generate the energy needed for cellular processes, most cancer cells instead rely on aerobic glycolysis, a phenomenon termed "the Warburg effect." Aerobic glycolysis is an inefficient way to generate adenosine 5'-triphosphate (ATP), however, and the advantage it confers to cancer cells has been unclear. Here we propose that the metabolism of cancer cells, and indeed all proliferating cells, is adapted to facilitate the uptake and incorporation of nutrients into the biomass (e.g., nucleotides, amino acids, and lipids) needed to produce a new cell. Supporting this idea are recent studies showing that (i) several signaling pathways implicated in cell proliferation also regulate metabolic pathways that incorporate nutrients into biomass; and that (ii) certain cancer-associated mutations enable cancer cells to acquire and metabolize nutrients in a manner conducive to proliferation rather than efficient ATP production. A better understanding of the mechanistic links between cellular metabolism and growth control may ultimately lead to better treatments for human cancer.
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              MicroRNAs: genomics, biogenesis, mechanism, and function.

              David P Bartel (2004)
              MicroRNAs (miRNAs) are endogenous approximately 22 nt RNAs that can play important regulatory roles in animals and plants by targeting mRNAs for cleavage or translational repression. Although they escaped notice until relatively recently, miRNAs comprise one of the more abundant classes of gene regulatory molecules in multicellular organisms and likely influence the output of many protein-coding genes.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cancer Manag Res
                Journal ID (iso-abbrev): Cancer Manag Res
                Journal ID (publisher-id): cmar
                Journal ID (pmc): cancmanres
                Title: Cancer Management and Research
                Publisher: Dove
                ISSN (Electronic): 1179-1322
                Publication date (Electronic): 05 July 2021
                Publication date Collection: 2021
                Volume: 13
                Pages: 5317-5336
                Affiliations
                [1 ]Reproductive & Women-Children Hospital, School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine , Chengdu, Sichuan, 611137, People’s Republic of China
                Author notes
                Correspondence: Linjiang Song; Chi Liu Reproductive & Women-Children Hospital, School of Medical and Life Sciences, Chengdu University of Traditional Chinese Medicine , Chengdu, Sichuan, 611137, People’s Republic of China Email linjsong_scu@163.com; liuchi1985@163.com
                Author information
                http://orcid.org/0000-0003-4102-946X
                http://orcid.org/0000-0002-0512-0410
                Article
                Publisher ID: 314502
                DOI: 10.2147/CMAR.S314502
                PMC ID: 8275123
                PubMed ID: 34262341
                SO-VID: 3cf600a9-0dd2-49c9-9dcb-a10df803003b
                Copyright © © 2021 Huang et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 06 April 2021
                Date accepted : 19 June 2021
                Page count
                Figures: 3, Tables: 2, References: 175, Pages: 20
                Funding
                Funded by: Foundation of Science and Technology Department of Sichuan Province;
                Funded by: Chengdu University of Traditional Chinese Medicine, open-funder-registry 10.13039/501100008402;
                Funded by: Postdoctoral Science Foundation of Chengdu University of Traditional Chinese Medicine;
                The work was supported by Foundation of Science and Technology Department of Sichuan Province (2020YJ0147); Foundation of “apricot grove scholar” of Chengdu University of Traditional Chinese Medicine (2019yky09); Postdoctoral Science Foundation of Chengdu University of Traditional Chinese Medicine (030054080).
                Categories
                Subject: Review

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna,cancer progression,glycolysis,signaling pathway
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: lncrna, cancer progression, glycolysis, signaling pathway

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