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miR-142:血液系统恶性肿瘤的主调控因子及治疗机会。

miR-142: A Master Regulator in Hematological Malignancies and Therapeutic Opportunities.

机构信息

Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.

Division of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medicine, New York, NY 10065, USA.

出版信息

Cells. 2023 Dec 30;13(1):84. doi: 10.3390/cells13010084.

DOI:10.3390/cells13010084
PMID:38201290
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10778542/
Abstract

MicroRNAs (miRNAs) are a type of non-coding RNA whose dysregulation is frequently associated with the onset and progression of human cancers. miR-142, an ultra-conserved miRNA with both active -3p and -5p mature strands and wide-ranging physiological targets, has been the subject of countless studies over the years. Due to its preferential expression in hematopoietic cells, miR-142 has been found to be associated with numerous types of lymphomas and leukemias. This review elucidates the multifaceted role of miR-142 in human physiology, its influence on hematopoiesis and hematopoietic cells, and its intriguing involvement in exosome-mediated miR-142 transport. Moreover, we offer a comprehensive exploration of the genetic and molecular landscape of the miR-142 genomic locus, highlighting its mutations and dysregulation within hematological malignancies. Finally, we discuss potential avenues for harnessing the therapeutic potential of miR-142 in the context of hematological malignancies.

摘要

微小 RNA(miRNA)是一种非编码 RNA,其失调通常与人类癌症的发生和发展有关。miR-142 是一种超保守的 miRNA,具有活跃的 -3p 和 -5p 成熟链以及广泛的生理靶标,多年来一直是无数研究的主题。由于其在造血细胞中的优先表达,miR-142 已被发现与多种类型的淋巴瘤和白血病有关。这篇综述阐明了 miR-142 在人类生理学中的多方面作用,它对造血和造血细胞的影响,以及它在细胞外体介导的 miR-142 运输中的有趣作用。此外,我们全面探讨了 miR-142 基因组位点的遗传和分子景观,强调了其在血液恶性肿瘤中的突变和失调。最后,我们讨论了在血液恶性肿瘤中利用 miR-142 的治疗潜力的潜在途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/7aefaa2033ac/cells-13-00084-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/0e9b63d1abf6/cells-13-00084-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/69ff20e55382/cells-13-00084-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/2bd81ccb6e93/cells-13-00084-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/7aefaa2033ac/cells-13-00084-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/0e9b63d1abf6/cells-13-00084-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/69ff20e55382/cells-13-00084-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/2bd81ccb6e93/cells-13-00084-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b84a/10778542/7aefaa2033ac/cells-13-00084-g004.jpg

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A gain-of-function mutation in microRNA 142 is sufficient to cause the development of T-cell leukemia in mice.
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