Abstract
Oxidative stress is a pathological condition determined by a disturbance in reactive oxygen species (ROS) homeostasis. Depending on the entity of the perturbation, normal cells can either restore equilibrium or activate pathways of cell death. On the contrary, cancer cells exploit this phenomenon to sustain a proliferative and aggressive phenotype. In fact, ROS overproduction or their reduced disposal influence all hallmarks of cancer, from genome instability to cell metabolism, angiogenesis, invasion and metastasis. A persistent state of oxidative stress can even initiate tumorigenesis. MicroRNAs (miRNAs) are small non coding RNAs with regulatory functions, which expression has been extensively proven to be dysregulated in cancer. Intuitively, miRNA transcription and biogenesis are affected by the oxidative status of the cell and, in some instances, they participate in defining it. Indeed, it is widely reported the role of miRNAs in regulating numerous factors involved in the ROS signaling pathways. Given that miRNA function and modulation relies on cell type or tumor, in order to delineate a clearer and more exhaustive picture, in this review we present a comprehensive overview of the literature concerning how miRNAs and ROS signaling interplay affects breast cancer progression.
Highlights
Reactive oxygen species (ROS) are oxygen-derived small molecules in the form of free radicals or non-radicals [1]
It was thought that these molecules were only metabolic waste, deleterious for nucleic acids, lipids and proteins; scientists, discovered that ROS are used by the cell as messages to activate different physiological signaling cascades [2,3]
This enzyme is the main redox master regulator; under oxidative stress, its inhibitor Kelch-like ECH-associated protein 1 (Keap1) undergoes a conformational change that allows Nuclear-erythroid-2-related factor 2 (NRF2) dissociation and consequent translocation to the nucleus, where it enhances the transcription of different ROS-counteracting agents [19,20]
Summary
Reactive oxygen species (ROS) are oxygen-derived small molecules in the form of free radicals (i.e., contains one or more unpaired electrons) or non-radicals [1]. In a biological system, the balance between the concentration of ROS and the activation of antioxidant mechanisms is finely tuned [4]. When this equilibrium lacks, the phenomenon of oxidative stress occurs, causing the alteration of intracellular molecules, such as DNA and RNA. A shift towards ROS production, triggers a wide range of cellular responses, even apoptosis or phagocytosis, depending on the amplitude of the shift. OCaSnacnedr cmelalisnarreeguulsautoarllsyainndapacthhrwonaiycssitnaflteueonfcoedxidbyatRivOeSsptrreosds,uwctihoinch(Ftihgeuyrea1r)e. aCbalnecteor ceexlplsloairtetuossuuaslltyaiinn aa pchrorolinfeicrasttiavtee oafnodxiadgagtriveesssitvreesps,hwenhoicthypthe.eyMaorreeaobvleert,odeuxepltooittthoesirusdteatinrima penrotalilfearcattiiovne,aRnOd Sagcgarnesaslisvoe ipnhiteinaotetytpuem. oMriogreenoveseirs, d[5u]e. tIot itshethirudseitmrimpoernttaanl tacntoiotnt,oRoOvSerclaonokalsthoeiniimtiaptaecttuomf osruigchenpehsiesn[o5m]. eItniosnthouns eimveproyrtcaenlltunlaort tporoocveesrsloaonkdt,hienipmaprtaicctuolafrs,uocnh tphhoesneocmruecnioanl foonr ethveerdyecveellluolpamr penrotcaenssdapnrdo,girnepssairotnicuolfaar, noenotphloasseticcrduicsieaalsfeo.r the development and progression of a neoplastic disease
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