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Volume 50 Number 1
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Volume 49 Number 3

Research articles

ScienceAsia 50 (2024):ID 2024021 1-10 |doi: 10.2306/scienceasia1513-1874.2024.021

MicroRNA-153-3p promotes hepatocellular carcinoma progression by modulating SPRY2 expression and the MAPK/ERK signalling pathway

Peihua Yuana, Zhiling Zhaoa, Wenjie Hua, Hongyang Lia, Jieying Liub,*, Luying Liua,*

ABSTRACT:     Hepatocellular carcinoma (HCC) is the most common primary liver cancer and among the most prevalent digestive system cancers. MicroRNAs (miRNAs) have been linked to multiple cellular processes, including cellular proliferation, differentiation, and cancer development. Although miRNA-153-3p participates in various malignancies, its role in HCC and its underlying mechanisms remain unclear. In this study, we investigated the expression and molecular mechanisms of miRNA-153-3p in HCC. miRNA-153-3p and SPRY2 expression was evaluated in human tissues and cell lines using quantitative PCR and western blotting. The cell proliferation, migration, and invasion capacities were assessed using Cell Counting Kit-8 and Transwell assays. The cell cycle and apoptosis were analysed using flow cytometry, and the relationship between miRNA-153-3p and SPRY2 was confirmed using a dual-luciferase reporter assay. miRNA-153-3p was upregulated, whereas SPRY2 was downregulated in HCC tissues compared with para-carcinoma tissues. Overexpression of miRNA-153-3p promotes HCC proliferation, migration, and invasion by targeting SPRY2 and mitogen-activated protein kinase/extracellular signal-regulated kinase signalling pathway-related proteins. It was also observed that SPRY2 overexpression partially rescued the effects of miRNA-153-3p. This study provides an experimental reference for identifying molecular targets for HCC therapy

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a Department of Pathology, Binzhou Medical University, Yantai, Shandong 264003 China
b Department of Physiology, Binzhou Medical University, Yantai, Shandong 264003 China

* Corresponding author, E-mail: liujybz@126.com, llixq@126.com

Received 19 Sep 2022, Accepted 10 Dec 2023