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miRNA PC-3p-2869 通过靶向 CDK8、EEF1A1 和 NTN1 调控鹿茸生长并抑制人骨肉瘤和软骨肉瘤细胞的增殖和迁移

MicroRNA PC-3p-2869 Regulates Antler Growth and Inhibits Proliferation and Migration of Human Osteosarcoma and Chondrosarcoma Cells by Targeting CDK8, EEF1A1, and NTN1.

机构信息

Laboratory of Genetics and Molecular Biology, College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, China.

Biotechnology Program, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.

出版信息

Int J Mol Sci. 2023 Jun 29;24(13):10840. doi: 10.3390/ijms241310840.

DOI:10.3390/ijms241310840
PMID:37446017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10341717/
Abstract

MicroRNAs (miRNAs) play a crucial role in maintaining the balance between the rapid growth and suppression of tumorigenesis during antler regeneration. This study investigated the role of a novel miRNA, PC-3p-2869 (miR-PC-2869), in antler growth and its therapeutic potential in human osteosarcoma and chondrosarcoma. Stem-loop RT-qPCR showed that miR-PC-2869 was expressed extensively in diverse layers of antler tissues. Overexpression of miR-PC-2869 suppressed the proliferation and migration of antler cartilage cells. Similarly, heterologous expression of miR-PC-2869 reduced the proliferation, colony formation, and migration of osteosarcoma cell line MG63 and U2OS and chondrosarcoma cell line SW1353. Moreover, 18 functional target genes of miR-PC-2869 in humans were identified based on the screening of the reporter library. Among them, 15 target genes, including CDK8, EEF1A1, and NTN1, possess conserved miR-PC-2869-binding sites between humans and red deer (). In line with this, miR-PC-2869 overexpression decreased the expression levels of CDK8, EEF1A1, and NTN1 in MG63, SW1353, and antler cartilage cells. As expected, the knockdown of CDK8, EEF1A1, or NTN1 inhibited the proliferation and migration of MG63, SW1353, and antler cartilage cells, demonstrating similar suppressive effects as miR-PC-2869 overexpression. Furthermore, we observed that CDK8, EEF1A1, and NTN1 mediated the regulation of c-myc and cyclin D1 by miR-PC-2869 in MG63, SW1353, and antler cartilage cells. Overall, our work uncovered the cellular functions and underlying molecular mechanism of antler-derived miR-PC-2869, highlighting its potential as a therapeutic candidate for bone cancer.

摘要

微小 RNA（miRNAs）在鹿茸再生过程中维持肿瘤发生的快速生长和抑制之间的平衡中起着至关重要的作用。本研究探讨了一种新型 miRNA，PC-3p-2869（miR-PC-2869），在鹿茸生长中的作用及其在人骨肉瘤和软骨肉瘤中的治疗潜力。茎环 RT-qPCR 显示 miR-PC-2869在鹿茸组织的不同层中广泛表达。miR-PC-2869 的过表达抑制了鹿茸软骨细胞的增殖和迁移。同样，miR-PC-2869 的异源表达降低了骨肉瘤细胞系 MG63 和 U2OS 以及软骨肉瘤细胞系 SW1353 的增殖、集落形成和迁移。此外，根据报告基因文库的筛选，鉴定了 miR-PC-2869 在人类中的 18 个功能靶基因。其中，包括 CDK8、EEF1A1 和 NTN1 在内的 15 个靶基因在人类和红鹿（）之间具有保守的 miR-PC-2869 结合位点。与此一致，miR-PC-2869 的过表达降低了 MG63、SW1353 和鹿茸软骨细胞中 CDK8、EEF1A1 和 NTN1 的表达水平。正如预期的那样，CDK8、EEF1A1 或 NTN1 的敲低抑制了 MG63、SW1353 和鹿茸软骨细胞的增殖和迁移，表现出与 miR-PC-2869 过表达相似的抑制作用。此外，我们观察到 CDK8、EEF1A1 和 NTN1 介导 miR-PC-2869 对 MG63、SW1353 和鹿茸软骨细胞中 c-myc 和 cyclin D1 的调节。总之，我们的工作揭示了鹿茸衍生的 miR-PC-2869 的细胞功能和潜在的分子机制，强调了其作为骨癌治疗候选物的潜力。

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