The Causes and Consequences of miR-503 Dysregulation and Its Impact on Cardiovascular Disease and Cancer

microRNAs (miRs) are short, non-coding RNAs that regulate gene expression by mRNA degradation or translational repression. Accumulated studies have demonstrated that miRs participate in various biological processes including cell differentiation, proliferation, apoptosis, metabolism and development,...

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Published inFrontiers in pharmacology Vol. 12; p. 629611
Main Authors He, Yanjing, Cai, Yin, Pai, Pearl Mingchu, Ren, Xinling, Xia, Zhengyuan
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 08.03.2021
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Summary:microRNAs (miRs) are short, non-coding RNAs that regulate gene expression by mRNA degradation or translational repression. Accumulated studies have demonstrated that miRs participate in various biological processes including cell differentiation, proliferation, apoptosis, metabolism and development, and the dysregulation of miRs expression are involved in different human diseases, such as neurological, cardiovascular disease and cancer. microRNA-503 (miR-503), one member of miR-16 family, has been studied widely in cardiovascular disease and cancer. In this review, we summarize and discuss the studies of miR-503 and , and how miR-503 regulates gene expression from different aspects of pathological processes of diseases, including carcinogenesis, angiogenesis, tissue fibrosis and oxidative stress; We will also discuss the mechanisms of dysregulation of miR-503, and whether miR-503 could be applied as a diagnostic marker or therapeutic target in cardiovascular disease or cancer.
Bibliography:Ana Karen González Palomo, Universidad Autónoma de San Luis Potosí, Mexico
Edited by: Chiranjib Chakraborty, Adamas University, India
This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology
Reviewed by: Anatoliy Ivashchenko, Al-Farabi Kazakh National University, Kazakhstan
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2021.629611