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Hsa_circ_0079480 通过 miR-654-3p/HDGF 轴促进急性髓系白血病的肿瘤进展。

Hsa_circ_0079480 promotes tumor progression in acute myeloid leukemia via miR-654-3p/HDGF axis.

机构信息

Department of Hematology, The First People’s Hospital of Shangqiu, Shangqiu 476100, Henan, China.

出版信息

Aging (Albany NY). 2020 Dec 3;13(1):1120-1131. doi: 10.18632/aging.202240.

DOI:10.18632/aging.202240
PMID:33290265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7835062/
Abstract

Circular RNAs (circRNAs) are newly-discovered endogenous non-coding RNAs that have vital functions in regulating gene expression in tumorigenesis. Nonetheless, the function of circRNAs in acute myeloid leukemia (AML) are not yet clarified. In this analysis, hsa_circ_0079480, a novel circRNA, has been identified as being highly expressed in AML. Loss-of-function assays showed that reduction of hsa_circ_0079480 decreased the growth and stimulated apoptosis of AML cells . Furthermore, miR-654-3p was sponged by hsa_circ_0079480, and hepatoma-derived growth factor (HDGF) was targeted by miR-654-3p with respect to the fundamental mechanism. Moreover, the influence on growth and apoptosis of AML cells stimulated by hsa_circ_0079480 inhibition can be rescued by miR-654-3p inhibitor or HDGF overexpression. In summary, hsa_circ_0079480 is highly expressed in AML and drives by tumor progression via regulation of hsa_circ_0079480/miR-654-3p/HDGF axis, indicating that hsa_circ_0079480 may function as a new treatment target for AML therapy.

摘要

环形 RNA(circRNAs)是新发现的内源性非编码 RNA,在肿瘤发生中对基因表达具有重要的调控作用。然而,circRNAs 在急性髓系白血病(AML)中的功能尚不清楚。在本分析中,hsa_circ_0079480,一种新型 circRNA,被鉴定为在 AML 中高度表达。功能丧失实验表明,hsa_circ_0079480 的减少降低了 AML 细胞的生长并刺激了细胞凋亡。此外,hsa_circ_0079480 可以吸附 miR-654-3p,而 miR-654-3p 可以靶向肝癌衍生生长因子(HDGF),这是其基本机制。此外,hsa_circ_0079480 抑制对 AML 细胞生长和凋亡的影响可以通过 miR-654-3p 抑制剂或 HDGF 过表达来挽救。总之,hsa_circ_0079480 在 AML 中高度表达,并通过调节 hsa_circ_0079480/miR-654-3p/HDGF 轴驱动肿瘤进展,表明 hsa_circ_0079480 可能作为 AML 治疗的新治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/76f16fa5efea/aging-13-202240-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/1af3cfe86fba/aging-13-202240-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/8a2839aa98cc/aging-13-202240-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/c569a0be9a78/aging-13-202240-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/e1c09ebedf8a/aging-13-202240-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/35b2d6945392/aging-13-202240-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/2e9fa98e5e4d/aging-13-202240-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/76f16fa5efea/aging-13-202240-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/1af3cfe86fba/aging-13-202240-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/8a2839aa98cc/aging-13-202240-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/c569a0be9a78/aging-13-202240-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/e1c09ebedf8a/aging-13-202240-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/35b2d6945392/aging-13-202240-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/2e9fa98e5e4d/aging-13-202240-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f1fd/7835062/76f16fa5efea/aging-13-202240-g007.jpg

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