Hydroxysafflor yellow a inhibits proliferation and migration of human hepatocellular carcinoma cells and promotes apoptosis via PI3K pathway
10.3781/j.issn.1000-7431.2018.11.161
- Author:
Haoran SONG
1
Author Information
1. Department of Human Anatomy and Organization Embryology, College of Basic Medicine, Binzhou Medical University
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cell proliferation;
Hydroxysafflor yellow A;
Liver neoplasms;
LY294002;
PI3K / Akt pathway
- From:
Tumor
2018;38(9):830-839
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of hydroxysafflor yellow A (HSYA) on the proliferation, apoptosis and migration of hepatocellular carcinoma cells, and to explore whether HSYA plays a role through phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB, Akt) signaling pathway. Methods: After the treatment with HSYA and PI3K inhibitor LY294002, CCK-8 assay, clone formation assay and scratch healing assay were used to detect the proliferation, clone formation and migration abilities of human hepatoma HepG2, Hep3B and SMMC7721 cells, respectively. FCM was used to detect the effect of HSYA on the apoptosis of HepG2 cells. Western blotting was used to detect the expressions of matrix metalloprotein 2 (MMP2), caspase 3, cleaved-caspase 3 and phospho-Akt (p-Akt). Results: Both 50 μmol/L HSYA and 10 μmol/L LY294002 inhibited the proliferation of human hepatoma HepG2, Hep3B and SMMC7721 cells (all P < 0.05). The clone formation rate and migration rate of HepG2, Hep3B and SMMC7721 cells treated with 50 μmol/L HSYA, 10 μmol/ L LY294002 and 50 μmol/L HSYA in combination with 10 μmol/L LY294002 were lower than those in the untreated control group (all P < 0.05). The clone formation rate and migration rate of HepG2, Hep3B and SMMC7721 cells in HSYA combined with LY294002 treatment group were lower than those in HSYA or LY294002 alone treatment group (all P < 0.01). The apoptosis rates of HepG2 cells in HSYA, LY294002 and HSYA combined with LY294002 treatment groups were higher than those in the untreated control group (all P < 0.05). The apoptosis rate of HepG2 cells in HSYA combined with LY294002 treatment group was higher than that in HSYA or LY294002 alone treatment group (P < 0.01). After the treatment with HSYA, LY294002 and HSYA combined with LY294002, the expression levels of p-Akt, MMP2 and caspase 3 in HepG2 cells were lower than those in the untreated control group (all P < 0.01), and the expression level of cleaved-caspase 3 was higher than that in the untreated control group (P < 0.01). The effects of HSYA combined with LY294002 treatment on the expressions of p-Akt, MMP2, caspase 3 and cleaved-caspase 3 were better than those of HSYA or LY294002 alone treatment group (all P < 0.01). Conclusion: HSYA can inhibit the proliferation and migration abilities of hepatocellular carcinoma HepG2, Hep3B and SMMC7721 cells, and induce the apoptosis of HepG2 cells by blocking PI3K/Akt signaling pathway.
