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Review
. 2020 Apr 22;21(8):2947.
doi: 10.3390/ijms21082947.

Crosstalk of lncRNA and Cellular Metabolism and Their Regulatory Mechanism in Cancer

Yang-Hsiang Lin  1   2
Affiliations
Review

Crosstalk of lncRNA and Cellular Metabolism and Their Regulatory Mechanism in Cancer

Yang-Hsiang Lin. Int J Mol Sci. .

Abstract

The imbalanced regulation of metabolic homeostasis and energy production is highly associated with inflammation, tumor growth, metastasis and cancer progression. Both glycolysis and oxidative phosphorylation maintain metabolic homeostasis and energy production in cells. Long noncoding RNAs (lncRNAs) are a class of non-protein-coding transcripts longer than 200 nucleotides. Furthermore, lncRNAs can function as either tumor suppressors or oncogenes in cancer. Dysregulated lncRNAs reportedly regulate cancer hallmarks such as tumor growth, metabolism and metastasis. Accordingly, uncovering the interaction between lncRNAs and cellular metabolism has become a necessity when attempting to identify effective therapeutic and preventive strategies in cancer progression. This review summarizes important knowledge of the actions of known lncRNAs-mediated cancer metabolism.

Keywords: cancer; glycolysis; lncRNA; mitochondria; therapeutic target.

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Conflict of interest statement

The author have no conflicts of interest to disclose.

Figures

Figure 1
Figure 1
Classifications and actions of Long noncoding RNAs (lncRNAs) in cancer. (A) A schematic diagram indicating the classification of lncRNAs according to their orientation and position, including intergenic, bidirectional sense, antisense, intronic lncRNAs and enhancer RNAs (eRNAs). The arrow represents the transcription direction. (B) The mechanisms of lncRNAs. Guides are lncRNAs that can recruit specific proteins to target genes, either in cis or in trans. Scaffolds are lncRNAs that can associate with multiple proteins to form ribonucleoprotein complexes. This complex may modulate histone modifications such as methylation. Decoys are lncRNAs that can bind to transcription factors or other proteins and are subsequently removed from a specific location. LncRNAs can function as microRNA (miRNA ) sponges to regulate cellular function. Enhancers act as cis-acting elements and contribute to increase the target genes expression.
Figure 2
Figure 2
Functional roles of lncRNA in tumor metabolism. LncRNAs regulate target gene-mediated glucose metabolism (A) and mitochondrial function (B) in cancer. The role of lncRNA-mediated liver kinase B1 (LKB1)/AMP-activated protein kinase (AMPK) pathways (C), hypoxia-inducible factor 1α (HIF1α) (D), and p53 (E) in tumor cells was shown.
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References

    1. Pavlova N.N., Thompson C.B. The Emerging Hallmarks of Cancer Metabolism. Cell Metab. 2016;23:27–47. doi: 10.1016/j.cmet.2015.12.006. - DOI - PMC - PubMed
    1. Liu J., Zhang C., Hu W., Feng Z. Tumor suppressor p53 and metabolism. J. Mol. Cell Biol. 2019;11:284–292. doi: 10.1093/jmcb/mjy070. - DOI - PMC - PubMed
    1. Stine Z.E., Walton Z.E., Altman B.J., Hsieh A.L., Dang C.V. MYC, Metabolism, and Cancer. Cancer Discov. 2015;5:1024–1039. doi: 10.1158/2159-8290.CD-15-0507. - DOI - PMC - PubMed
    1. Corcoran S.E., O’Neill L.A. HIF1alpha and metabolic reprogramming in inflammation. J. Clin. Investig. 2016;126:3699–3707. doi: 10.1172/JCI84431. - DOI - PMC - PubMed
    1. Wolf A., Agnihotri S., Micallef J., Mukherjee J., Sabha N., Cairns R., Hawkins C., Guha A. Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme. J. Exp. Med. 2011;208:313–326. doi: 10.1084/jem.20101470. - DOI - PMC - PubMed

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