Abstract
Reactive oxygen species (ROS) are highly reactive oxygen-containing chemical species formed as a by-product of normal aerobic respiration and also from a number of other cellular enzymatic reactions. ROS function as key mediators of cellular signaling pathways involved in proliferation, survival, apoptosis, and immune response. However, elevated and sustained ROS production promotes tumor initiation by inducing DNA damage or mutation and activates oncogenic signaling pathways to promote cancer progression. Recent studies have shown that ROS can facilitate carcinogenesis by controlling microRNA (miRNA) expression through regulating miRNA biogenesis, transcription, and epigenetic modifications. Likewise, miRNAs have been shown to control cellular ROS homeostasis by regulating the expression of proteins involved in ROS production and elimination. In this review, we summarized the significance of ROS in cancer initiation, progression, and the regulatory crosstalk between ROS and miRNAs in cancer.
Highlights
Reactive oxygen species (ROS) are free radicals, ions, or molecules with a single unpaired electron
These findings indicate that ROS can act as a double-edged sword, both overproduction or inhibition of ROS can have a significant effect on cancer progression
These findings suggest that the endogenous expression of endogenous antioxidants is crucial for the prevention of cellular ROS accumulation, which is manipulated by miRNAs in cancer cells to support cancer progression
Summary
Reactive oxygen species (ROS) are free radicals, ions, or molecules with a single unpaired electron. MicroRNAs (miRNAs) are a class of small non-coding RNAs that are approximately 22 nucleotides long and regulate gene expression at the post-transcriptional level [10]. They regulate gene expression by binding to the target messenger RNA (mRNA) transcript which activates either degradation or translation suppression based on the extent of basepairing. Another study has shown that miR-30e regulates oxidative stress and ROS levels by targeting SNAI1 mRNA in human umbilical endothelial vein cells [14]. These findings suggest that ROS and miRNAs may co-regulate each other in cancer to maintain cellular ROS levels that support cancer development. We discuss the significance of ROS in cancer development, as well as the crosstalk between ROS and miRNAs in the regulation of redox homeostasis and cancer progression
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