Silencing AEBP2 Inhibits the Proliferation and Migration of Hepatocellular Carcinoma Cells via the PI3K/Akt Signaling Pathway
10.13865/j.cnki.cjbmb.2022.04.1647
- Author:
Cai-Yun LUO
1
;
Zhi-Rui ZENG
1
;
Shan LEI
1
;
Qiang ZHANG
1
;
Da-Quan SUN
1
;
Ji-Gang PAN
1
;
Guo-Qiang XU
1
Author Information
1. School of Basic Medical Sciences, Guizhou Medical University
- Publication Type:Journal Article
- Keywords:
adipocyte enhancer binding protein 2 (AEBP2);
hepatocellular carcinoma cells (HCC);
invasion;
migration;
PI3K/Akt signaling pathway
- From:
Chinese Journal of Biochemistry and Molecular Biology
2022;38(6):789-798
- CountryChina
- Language:Chinese
-
Abstract:
Adipocyte enhancer binding protein 2, as a component protein of Polycomb repressive complex (PRC2), is involved in the proliferation and migration of many tumor cells. However, its role in HCC is still unclear. In this study, we identify that AEBP2 was upregulated in HCC samples from the UALCAN and Kaplan-Meier Plotter database, which was correlated to the overall survival time of HCC patients. Real-time quantitative PCR and Western blotting confirmed that the expression of AEBP2 in HCC cells was higher than normal liver cells. After silencing AEBP2 in HepG2 and Huh-7 cells, the effects of the proliferation, apoptosis, migration and invasion were detected by colony formation, CCK-8, flow cytometry, scratch healing and Transwell chamber, respectively. Compared with the control group, down-regulation of AEBP2 expression inhibited the proliferation, migration and invasion in HepG2 and Huh-7 cells, as well as promoted apoptosis (P<0. 05). Immunofluorescence and Western blotting results showed that AEBP2 silencing inhibited epithelial-mesenchymal transformation (EMT) (P < 0. 05). Bioinformatics analysis showed that AEBP2 is involved the PI3K/Akt signaling pathway. Western blotting results confirmed that silencing AEBP2 down-regulated the expression levels of PI3K, p-AKT (S473), mTOR, MMP-2 and MMP-9 proteins (P<0. 05). In addition, the effects of AEBP2 silencing on HepG2 cells migration and invasion could be reversed by PI3K/Akt pathway agonist insulin-like Growth Factors (IGF-1) (P < 0. 01). In summary, our study showed that AEBP2 promoted the proliferation and migration of HCC cell by regulating PI3K/AKT pathway. This study provided a theoretical basis for the role of AEBP2 in HCC.
