MicroRNA miR-124-3p suppresses proliferation and epithelial–mesenchymal transition of hepatocellular carcinoma via ARRDC1 (arrestin domain containing 1). Issue 4 (1st April 2022)

• Record Type: Journal Article
• Authors: Zhao, Qiannan; Jiang, Fen; Zhuang, Hui; Chu, Yanfeng; Zhang, Fang; Wang, Chenghong
• Is Part Of: Bioengineered. Volume 13:Issue 4(2022)
• Page Start: 8255
• Page End: 8265
• Publication Date: 2022-04-01
• Subjects: microRNA -- hepatocellular carcinoma -- proliferation -- epithelial–mesenchymal transition; Biomedical engineering -- Periodicals; Biotechnology -- Periodicals; Microbiology -- Periodicals; 660.6
• DOI: 10.1080/21655979.2022.2051686
• Languages: English
• ISSNs: 2165-5987

Abstract

ABSTRACT: Hepatocellular carcinoma (HCC) is responsible for high morbidity and mortality worldwide. Increasing evidence suggests that microRNAs intensively participate in HCC development and progression. In the current study, we aimed to explore the impact of miR-124-3p in the proliferation and epithelial–mesenchymal transition (EMT) of HCC. The RT-qPCR assay was employed to determine miR-124-3p expression in human HCC specimens and cell lines. Luciferase assay was used to validate the miR-124-3p target gene. Western Blot and RT-qPCR were performed to study the effects of miR-124-3p modulation on ARRDC1 (Arrestin Domain Containing 1) mRNA and protein expressions. MTT assay, wound healing assay, EdU assay, and Transwell assay were utilized to verify the impact of miR-144-3p modulation on HCC proliferation and EMT via ARRDC1. We found that MiR-124-3p expression downregulates in HCC. Overexpression of miR-124-3p reduced the HCC cell proliferation and EMT. Meanwhile, we determined that the expression of ARRDC1 is increased in HCC, and miR-124-3p directly binds the 3ʹUTR of ARRDC1 and inhibits its expression at mRNA and protein level, suggesting that miR-124-3p was capable of negatively modulating ARRDC1. Besides, cotransfection of ARRDC1-overexpression plasmid and miR-124-3p mimics increased the cell proliferation and EMT as compared to miR-124-3p mimics. Our study concluded that miR-124-3p directly binds the 3ʹUTR of ARRDC1 and exerts anti-tumorous effects by inhibiting the HCC proliferation and EMT. Therefore, miR-124-3p/ARRDC1 axis may serve as a novel therapeutic target to inhibit HCC growth and metastasis. Graphical Abstract: uf0001