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Updated: Jan 30, 2026

Preparation and In Vitro Characterization of Magnetized miR-modified Endothelial Cells
Published on: May 2, 2017
miR-424-5p Regulates Hepatoma Cell Proliferation and Apoptosis
Lianshu Piao1, Fei Wang1, Yanyan Wang1
1Department of Gastroenterology, Affiliated Zhongshan Hospital of Dalian University, Dalian, China.
Objective:
Yes-associated protein (Yes-associated protein 1 [YAP1]) is an important oncogene that is related to the pathogenesis and progression of liver cancer. It was found that miR-424-5p expression was significantly decreased in liver cancer tissues, revealing its anticancer effect. Bioinformatic analysis demonstrated the targeted relationship between miR-424-5p and the 3' untranslated region of YAP1. This study investigated the role of miR-424-5p in regulating YAP1 expression and affecting hepatoma cell proliferation and apoptosis.
Materials And Methods:
Tumors and normal liver tissues adjacent to tumors were collected from patients to detect the expression of miR-424-5p and YAP1. A dual-luciferase reporter gene assay was adopted to explore the targeted regulation between miR-424-5p and YAP1. Liver cancer HCCLM3 and MHCC97-L cells and normal liver HL-7702 cells were cultured in vitro to compare expression levels of miR-424-5p and YAP1. HCCLM3 and MHCC97-L cells were divided into the miR-NC group and miR-424-5p mimic group. Cell apoptosis was detected by flow cytometry. Cell proliferation was determined by EdU staining.
Results:
Compared with normal liver tissue, miR-424-5p expression was significantly decreased, while YAP1 mRNA and protein levels were obviously upregulated in liver cancer tissues, which were related to the clinical stage. A negative correlation was found between miR-424-5p and YAP1 mRNA levels in liver cancer tissues. Dual-luciferase reporter gene assay confirmed the targeted relationship between miR-424-5p and YAP1. miR-424-5p expression in HCCLM3 and MHCC97-L cells decreased compared with L20 cells, which correlated with malignancy. YAP1 level in HCCLM3 and MHCC97-L cells was significantly enhanced, which correlated with malignancy. miR-424-5p mimic transfection significantly downregulated YAP1 expression in HCCLM3 and MHCC97-L cells, resulting in enhanced apoptosis and attenuated cell proliferation.
Conclusions:
Decreased miR-424-5p expression and increased YAP1 expression are found in patients with liver cancer. Increased miR-424-5p can inhibit YAP1 expression, attenuate hepatoma cell proliferation, and induce cell apoptosis.
Insights
Reduced miR-424-5p expression is linked to increased Yes-associated protein 1 (YAP1) in liver cancer. Restoring miR-424-5p inhibits YAP1, reducing hepatoma cell proliferation and promoting apoptosis.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Yes-associated protein 1 (YAP1) is a key oncogene in liver cancer pathogenesis and progression.
- MicroRNA (miR)-424-5p expression is significantly reduced in liver cancer tissues, suggesting an anticancer role.
Purpose of the Study:
- To investigate the regulatory relationship between miR-424-5p and YAP1 in liver cancer.
- To determine the effect of miR-424-5p on hepatoma cell proliferation and apoptosis.
Main Methods:
- Analysis of miR-424-5p and YAP1 expression in patient tissues and cell lines.
- Dual-luciferase reporter gene assay to confirm direct targeting of YAP1 by miR-424-5p.
- In vitro experiments using miR-424-5p mimics to assess effects on cell proliferation and apoptosis.
Main Results:
- Liver cancer tissues and cells exhibit decreased miR-424-5p and increased YAP1 expression, correlating with clinical stage and malignancy.
- A negative correlation was observed between miR-424-5p and YAP1 levels.
- miR-424-5p mimic transfection suppressed YAP1 expression, reduced cell proliferation, and induced apoptosis in hepatoma cells.
Conclusions:
- Downregulation of miR-424-5p and upregulation of YAP1 are characteristic of liver cancer.
- Increasing miR-424-5p expression can suppress YAP1, inhibit hepatoma cell proliferation, and induce apoptosis, highlighting its therapeutic potential.
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