Abstract
Imbalanced regulation of reactive oxygen species (ROS) and antioxidant factors in cells is known as “oxidative stress (OS)”. OS regulates key cellular physiological responses through signal transduction, transcription factors and noncoding RNAs (ncRNAs). Increasing evidence indicates that continued OS can cause chronic inflammation, which in turn contributes to cardiovascular and neurological diseases and cancer development. MicroRNAs (miRNAs) are small ncRNAs that produce functional 18-25-nucleotide RNA molecules that play critical roles in the regulation of target gene expression by binding to complementary regions of the mRNA and regulating mRNA degradation or inhibiting translation. Furthermore, miRNAs function as either tumor suppressors or oncogenes in cancer. Dysregulated miRNAs reportedly modulate cancer hallmarks such as metastasis, angiogenesis, apoptosis and tumor growth. Notably, miRNAs are involved in ROS production or ROS-mediated function. Accordingly, investigating the interaction between ROS and miRNAs has become an important endeavor that is expected to aid in the development of effective treatment/prevention strategies for cancer. This review provides a summary of the essential properties and functional roles of known miRNAs associated with OS in cancers.
Highlights
Imbalanced regulation of reactive oxygen species (ROS) and antioxidant factors in cells is known as “oxidative stress (OS)” (Figure 1)
Excessive ROS production was identified in several cancers where they were significantly correlated with tumorigenesis
Cellular senescence is characterized by the expression of senescence-associated β-galactosidase (SA-β-gal), overexpression of the cyclin-dependent kinase (CDK) inhibitor, senescence-associated secretory phenotype (SASP), telomere shortening and persistent DNA damage response (DDR) [114]
Summary
Imbalanced regulation of reactive oxygen species (ROS) and antioxidant factors in cells is known as “oxidative stress (OS)” (Figure 1). Previous studies have demonstrated that miRNAs are significantly associated with tumor growth, metastasis and cancer progression [5,6]. A previous study indicated that miR-21 regulated ROS homeostasis and suppressed the antioxidant response in human umbilical vein endothelial cells (HUVECs) [10]. These findings suggest that ROS could be upstream regulators or downstream effectors of miRNAs. In this review, we focus on how ROS affect biological phenotypes through miRNA and how miRNAs regulate ROS-mediated function in cancer
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