Abstract
Cancer represents a complex disease originated from alterations in several genes leading to disturbances in important signaling pathways in tumor biology, favoring heterogeneity that promotes adaptability and pharmacological resistance of tumor cells. Metabolic reprogramming has emerged as an important hallmark of cancer characterized by the presence of aerobic glycolysis, increased glutaminolysis and fatty acid biosynthesis, as well as an altered mitochondrial energy production. The metabolic switches that support energetic requirements of cancer cells are closely related to either activation of oncogenes or down-modulation of tumor-suppressor genes, finally leading to dysregulation of cell proliferation, metastasis and drug resistance signals. Non-coding RNAs (ncRNAs) have emerged as one important kind of molecules that can regulate altered genes contributing, to the establishment of metabolic reprogramming. Moreover, diverse metabolic signals can regulate ncRNA expression and activity at genetic, transcriptional, or epigenetic levels. The regulatory landscape of ncRNAs may provide a new approach for understanding and treatment of different types of malignancies. In this review we discuss the regulatory role exerted by ncRNAs on metabolic enzymes and pathways involved in glucose, lipid, and amino acid metabolism. We also review how metabolic stress conditions and tumoral microenvironment influence ncRNA expression and activity. Furthermore, we comment on the therapeutic potential of metabolism-related ncRNAs in cancer.
Highlights
Specialty section: This article was submitted to Systems Biology, a section of the journal Frontiers in Physiology
Metabolic reprogramming has emerged as an important hallmark of cancer characterized by the presence of aerobic glycolysis, increased glutaminolysis and fatty acid biosynthesis, as well as an altered mitochondrial energy production
The metabolic switches that support energetic requirements of cancer cells are closely related to either activation of oncogenes or down-modulation of tumor-suppressor genes, leading to dysregulation of cell proliferation, metastasis and drug resistance signals
Summary
Akt: stimulates glycolysis by increasing expression of glucose transporters and glycolytic enzymes miR-451. IGF-I/insulin signaling: increased expression of genes involved in the regulation of glucose metabolism and mitochondrial function miR-7 miR-126 miR-33a/b. Inhibits cellular growth and glucose metabolism by regulating the IGF-1R/Akt signaling pathway. Regulates IRS1, an adaptor protein mediating IGF-I/insulin signaling, leading to activation of the PI3K, Akt and Ras-MAPK pathways. Represses AMP-activated kinase 1 (Ampkα1) and sirtuin 6 (Sirt6), involved in the regulation of lipid and glucose metabolism. 2011 c-Myc: The oncogene deregulates glycolysis through the activation of several components of the glucose metabolic pathway. LncRNA PCGEM1 c-Myc transcriptionally represses miR-23a/b, which targets glutaminase (GLS) inducing mitochondrial dysfunction. Stimulates the uptake of glucose by aerobic glycolysis and interacts directly with c-Myc, and enhances its transactivation activity by its recruitment to chromatin
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