Abstract
Oxidative stress refers to an imbalance between reactive oxygen species (ROS) generation and body's capability to detoxify the reactive mediators or to fix the relating damage. MicroRNAs are considered to be important mediators that play essential roles in the regulation of diverse aspects of carcinogenesis. Growing studies have demonstrated that the ROS can regulate microRNA biogenesis and expression mainly through modulating biogenesis course, transcription factors, and epigenetic changes. On the other hand, microRNAs may in turn modulate the redox signaling pathways, altering their integrity, stability, and functionality, thus contributing to the pathogenesis of multiple diseases. Both ROS and microRNAs have been identified to be important regulators and potential therapeutic targets in cancers. However, the information about the interplay between oxidative stress and microRNA regulation is still limited. The present review is aimed at summarizing the current understanding of molecular crosstalk between microRNAs and the generation of ROS in the pathogenesis of cancer.
Highlights
Reactive oxygen species (ROS), mainly including hydroxyl radicals (HO·), superoxide (O2·-), and hydrogen peroxide (H2O2), are usually generated under physiological conditions and have essential functions in living organisms [1,2,3]
Disruption of normal redox state, either because of excessive amounts of ROS or dysfunction of antioxidant defense system, would result in toxic damages through the production of free radicals and peroxides, give rise to pathophysiological situation that lead to multiple diseases, including cancer [3, 5]
Under persistent oxidative stress circumstances, cancer cells may evolve a particular set of adaptive mechanisms, which enhance ROS scavenging systems to deal with the stress and suppress cell apoptosis
Summary
Reactive oxygen species (ROS), mainly including hydroxyl radicals (HO·), superoxide (O2·-), and hydrogen peroxide (H2O2), are usually generated under physiological conditions and have essential functions in living organisms [1,2,3]. Nrf: nuclear factor E2-related factor 2; Keap: Kelch-like ECH-associated protein 1; HO-1: heme oxygenase-1; PRXL2A: peroxiredoxin-like 2A; ATG-5: autophagy-related 5; PDHX: pyruvate dehydrogenase complex component X; Mn-SOD: manganese superoxide dismutase; Gpx: glutathione peroxidase 2; TrxR2: thioredoxin reductase 2; ISCU: iron-sulfur cluster assembly enzyme; BBC3: BCL2-binding component 3; BTG2: BTG antiproliferation factor 2; MOMP: mitochondrial outer membrane permeabilization; ARHGAP10: Rho GTPase-activating protein 10; AKAP1: A-kinase anchoring protein 1; PPARGC1A: PPARG coactivator 1 alpha; ACACA: acetyl-CoA carboxylase alpha; FASN: fatty acid synthase; HMGCR: 3-hydroxy-3-methylglutaryl-CoA reductase; CYP27B1: cytochrome P450 family 27 subfamily B member 1; T-AOC: total antioxidation competence; SOD: superoxide dismutase; CAT: catalase; PDCD4: programmed cell death 4 protein; DCK: deoxycytidine kinase; WSB1: WD repeat and SOCS box containing 1; STAT3: signal transducer and activator of transcription 3; VEGF: vascular endothelial growth factor. Meng and colleagues investigated that miR-212 could directly target and downregulate Mn-SOD mRNA expression, thereby suppressing Mn-SOD-induced colorectal cancer metastasis [49] (Table 1)
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