Effects of MAGED4 overexpression on proliferation， migration， and adhesion of hepatocellular carcinoma
10.19405/j.cnki.issn1000–1492.2026.09.007
- VernacularTitle:MAGED4过表达对肝细胞癌增殖、迁移及黏附功能的影响
- Author:
Sheng ZHANG
1
;
Zhibi ZHANG
1
;
Xiaoqing YU
1
;
Xiaoqiong ZOU
1
;
Yuhang LIU
1
;
Hao LÜ
1
;
Feng LI
1
;
Yanjing WANG
1
;
Bin LUO
1
;
Xiaoxun XIE
1
;
Qingmei ZHANG
1
Author Information
1. Histology and Embryology， Guangxi Medical University，Nanning 530021
- Publication Type:Journal Article
- Keywords:
MAGED4;
hepatocellular carcinoma;
overexpression;
proliferation;
migration;
adhesion
- From:
Acta Universitatis Medicinalis Anhui
2026;61(9):1558-1567
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the impact of melanoma-associated antigen D4 （MAGED4） on the malignant biological behavior of hepatocellular carcinoma （HCC）， providing experimental evidence for its evaluation as a potential therapeutic target in HCC. MethodsGenes positively correlated with MAGED4 expression in HCC were screened using the LinkedOmics database， followed by GO functional and KEGG pathway enrichment analyses. Endogenously low-expressing SMMC-7721 and Huh7 cells were selected， with normal hepatic LO2 cells serving as controls. Stable overexpression cell lines were established via lentiviral infection （MAGED4 overexpression group）， with RT-PCR and Western blot validating overexpression efficiency. The effects of MAGED4 overexpression on cell proliferation， cell cycle distribution， migration， and adhesion were systematically analyzed using CCK-8 assays， flow cytometry， scratch healing assays， Transwell migration assays， and cell adhesion assays. ResultsBioinformatics analysis indicated that MAGED4 co-expressed genes were significantly enriched in biological processes closely associated with tumor proliferation and metastasis， including cell-cell adhesion， extracellular matrix organization， and the PI3K-Akt signaling pathway. A stable MAGED4 overexpression cell model was successfully established. In vitro functional assays demonstrated that MAGED4-overexpressing SMMC-7721 and Huh7 cells exhibited a mesenchymal-like morphology， whereas LO2 cells maintained an epithelial-like morphology. Compared with the empty-virus control groups， the MAGED4-overexpressing groups showed significantly increased proliferative activity （48 h： t=3.887， 22.070， 8.866， all P<0.05； 72 h： t=3.231， 23.840， 9.848， all P<0.05； 96 h： t=5.123， 49.800， 5.909， P<0.05， P<0.01， P<0.05）， wound healing rates （12 h： F=40.90， 44.00， 200.50， all P<0.001； 24 h： F=112.00， 34.89， 249.20， all P<0.001）， and numbers of migrated cells （F=239.20， 59.79， 132.80， all P<0.001）， along with significantly decreased numbers of adherent cells （F=73.65， 85.91， 138.00， all P<0.001）， while no significant differences were observed in cell cycle phase distribution in all three cell lines. ConclusionMAGED4 enhances proliferation and migration while suppressing adhesion in both HCC and normal hepatocytes， however， induces mesenchymal-like morphological changes exclusively in HCC cells， suggesting that MAGED4 is capable of driving HCC progression and may serve as a potential therapeutic target for HCC.
