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Review
. 2022 Mar 9:12:830420.
doi: 10.3389/fonc.2022.830420. eCollection 2022.

miR-484: A Potential Biomarker in Health and Disease

Affiliations
Review

miR-484: A Potential Biomarker in Health and Disease

Yin-Zhao Jia et al. Front Oncol. .

Abstract

Disorders of miR-484 expression are observed in cancer, different diseases or pathological states. There is accumulating evidence that miR-484 plays an essential role in the development as well as the regression of different diseases, and miR-484 has been reported as a key regulator of common cancer and non-cancer diseases. The miR-484 targets that have effects on inflammation, apoptosis and mitochondrial function include SMAD7, Fis1, YAP1 and BCL2L13. For cancer, identified targets include VEGFB, VEGFR2, MAP2, MMP14, HNF1A, TUSC5 and KLF12. The effects of miR-484 on these targets have been documented separately. Moreover, miR-484 is typically described as an oncosuppressor, but this claim is simplistic and one-sided. This review will combine relevant basic and clinical studies to find that miR-484 promotes tumorigenesis and metastasis in liver, prostate and lung tissues. It will provide a basis for the possible mechanisms of miR-484 in early tumor diagnosis, prognosis determination, disease assessment, and as a potential therapeutic target for tumors.

Keywords: apoptosis; cancer; metastasis; physiological conditions; proliferation.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
The sequence structure of the miR-484. Hsa-miR-484, mmu-miR-484 and rno-miR-484 are located on chromosome 16 (chr16: 15643294-15643372), chromosome 16 (chr16: 14159626-14159692) and chromosome 10(chr10: 27845-27921and 908408-908484). They all have the same and only one miR-484 mature sequence.
Figure 2
Figure 2
Prediction of miR-484 downstream targets and the role of miR-484 in physiological states. (A) The Wayne diagram shows the results of hsa-miR-484 and mus-miR-484 target prediction by four miRNA-related databases. In addition, a cross-set of common downstream targets for mouse and human. Left: hsa-miR-484 predicted target results. Right: mus-miR-484 predicted targets. Middle top: cross-set of three databases common to human (blue) and mouse (red) targets. Middle bottom: cross-set of four databases common to human (blue) and mouse (red) targets. (B) Mockup shows the mechanism of miR-484 involvement in maintaining the function of Ecs. (C) The mechanism of miR-484 involvement in mitochondrial function division in cardiomyocytes.
Figure 3
Figure 3
Effects of miR-484 target genes in apoptosis, tumorigenesis, and tumor drug resistance. miR-484 inhibits the tumorigenic process by suppressing the expression of ZEB1, SMAD2, HNF1A, MMP14, MAP2, PSMG1, SMAD9, MAGI1, and TBL1X. miR-484 targets SMAD7, YAP1, Fis1 BCL2L13, CD137L, Apaf-1, CCL18 and Wnt8a to affect the level of apoptosis. In addition, miR-484 regulates chemoresistance of cancer cells by targeting CDA, KLF-4, VEGFB and VEGFR1. Potential targets are screened and predicted through a database.
Figure 4
Figure 4
Role of miR-484 and its target genes on cancer cell biology. Different cell types or tissues regulate miR-484 mainly by LncRNA competitive repression and epigenetic mechanisms. miR-484 exerts oncogenic or pro-carcinogenic effects in different cancers by targeting genes related to cell proliferation and apoptosis.

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References

    1. Eulalio A, Huntzinger E, Izaurralde E. Getting to the Root of miRNA-Mediated Gene Silencing. Cell (2008) 132(1):9–14. doi: 10.1016/j.cell.2007.12.024 - DOI - PubMed
    1. Avital G, Franca GS, Yanai I. Bimodal Evolutionary Developmental miRNA Program in Animal Embryogenesis. Mol Biol Evol (2018) 35(3):646–54. doi: 10.1093/molbev/msx316 - DOI - PubMed
    1. Knauss JL, Bian S, Sun T. Plasmid-Based Target Protectors Allow Specific Blockade of miRNA Silencing Activity in Mammalian Developmental Systems. Front Cell Neurosci (2013) 7:163. doi: 10.3389/fncel.2013.00163 - DOI - PMC - PubMed
    1. Pasquariello R, Manzoni E, Fiandanese N, Viglino A, Pocar P, Brevini T, et al. . Implications of miRNA Expression Pattern in Bovine Oocytes and Follicular Fluids for Developmental Competence. Theriogenology (2020) 145:77–85. doi: 10.1016/j.theriogenology.2020.01.027 - DOI - PubMed
    1. Meganathan K, Jagtap S, Srinivasan SP, Wagh V, Hescheler J, Hengstler J, et al. . Neuronal Developmental Gene and miRNA Signatures Induced by Histone Deacetylase Inhibitors in Human Embryonic Stem Cells. Cell Death Dis (2015) 6:e1756. doi: 10.1038/cddis.2015.121 - DOI - PMC - PubMed

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