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Review
. 2022 Oct 1;17(1):26.
doi: 10.1186/s13062-022-00341-x.

Long non-coding RNAs affecting cell metabolism in cancer

Massimiliano Agostini  1 , Mara Mancini  2 , Eleonora Candi  3   4
Affiliations
Review

Long non-coding RNAs affecting cell metabolism in cancer

Massimiliano Agostini et al. Biol Direct. .

Abstract

Metabolic reprogramming is commonly recognized as one important hallmark of cancers. Cancer cells present significant alteration of glucose metabolism, oxidative phosphorylation, and lipid metabolism. Recent findings demonstrated that long non-coding RNAs control cancer development and progression by modulating cell metabolism. Here, we give an overview of breast cancer metabolic reprogramming and the role of long non-coding RNAs in driving cancer-specific metabolic alteration.

Keywords: Breast cancer; Cell metabolism; Long non-coding RNAs.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
LncRNA regulates glycolysis in breast cancer cells. A YAP regulate the expression of the lncRNA BCAR4, which in turn by interacting with GLI2, promotes the transcription of two enzymes, HK2 and PFKFB3, resulting in the upregulation of the glycolytic pathway. B Under hypoxic conditions the LncRNA HIFAL is essential for maintaining HIF-1α transactivation and stimulates glycolysis in breast cancer cells by regulating the expression of glycolytic genes. HK-2: hexokinase 2; PFKB3: 6-Phosphofructo-2-Kinase/Fructose-2,6-Biphosphatase 3; GLUT1: Glucose Transporter 1; LDHA: Lactate Dehydrogenase A; PDK1: Pyruvate Dehydrogenase Kinase 1; GLI2: GLI Family Zinc Finger 2
Fig. 2
Fig. 2
Regulation of mitochondrial activity and lipid metabolism by LncRNA in breast cancer. Energy–stress induces the expression of GAS5, which in turn inhibits the interaction between of FH, MDH2 and CS. This results in the reduction of TCA flux. The lncRNA NEAT stimulate the use of free fatty acids as energy source in breast cancer. NEAT1, sponging miR107, up regulates CPT1A expression in breast cancer cells. Competing with miR34a-5p and miR204-5p NEAT1 also controls the expression of ACSL4. TCA: Tricarboxylic acid; FH: Fumarate hydratase; CS: Citrate synthase; MDH2: Malate dehydrogenase; FAO: Fatty acid oxidation; ACSL4: Acyl-CoA Synthetase Long Chain Family Member 4; CPT1: Carnitine Palmitoyltransferase 1
See this image and copyright information in PMC

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