Abstract
Compared with normal cells, tumor cells display distinct metabolic characteristics. Long non-coding RNAs (lncRNAs), a large class of regulatory RNA molecules with limited or no protein-coding capacity, play key roles in tumorigenesis and progression. Recent advances have revealed that lncRNAs play a vital role in cell metabolism by regulating the reprogramming of the metabolic pathways in cancer cells. LncRNAs could regulate various metabolic enzymes that integrate cell malignant transformation and metabolic reprogramming. In addition to the known functions of lncRNAs in regulating glycolysis and glucose homeostasis, recent studies also implicate lncRNAs in amino acid and lipid metabolism. These observations reveal the high complexity of the malignant metabolism. Elucidating the metabolic-related functions of lncRNAs will provide a better understanding of the regulatory mechanisms of metabolism and thus may provide insights for the clinical development of cancer diagnostics, prognostics and therapeutics.
Highlights
Metabolism is the set of life-sustaining chemical transformations within the cells of organisms
By directly binding with lipin 2, SPRY4-IT1 downregulates the expression of diacylglycerol O-acyltransferase 2 (DGAT2), acyl carnitine, fatty acyl chains, and triacylglycerol, thereby leading to cellular lipotoxicity and functioning as an oncogene in human melanoma cells, which provides novel insight into the mechanisms by which extranuclear processing of Long non-coding RNAs (lncRNAs) contributes to lipid metabolism [80]
The mechanism underlying the A novel large antisense noncoding RNA (ANRIL)-dependent enhancement of nasopharyngeal carcinoma (NPC) progression may involve the ANRIL-induced phosphorylation of Akt and activate the mTOR pathway, which further upregulates the expression of GLUT1 and LDHA and promotes NPC development [138]
Summary
Metabolism is the set of life-sustaining chemical transformations within the cells of organisms. By activating the AKT/mTOR signal, ANRIL upregulates GLUT1 and LDHA expression, increasing glucose uptake and promoting cancer progression in NPC cells [40].
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