Inhibitory effect of epigallocatechin-3-gallate on human osteosarcoma cell line 143B and its underlying mechanism
10.3781/j.issn1000-7431.2017.11.091
- Author:
Chaoqun DONG
1
Author Information
1. Department of Orthopaedics, Childrens Hospital of Chongqing Medical University, Key Laboratory of Child Development and Disorders
- Publication Type:Journal Article
- Keywords:
Cell migration assays;
Cell proliferation;
Epigallocatechin-3-gallate;
Osteoscarcoma;
Wnt/β-catenin signaling pathway
- From:
Tumor
2017;37(6):568-575
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the inhibitory effect of epigallocatechin-3-gallate (EGCG) on human osteoscarcoma cell line 143B, and its possible molecular mechanism. Methods: Human osteoscarcoma 143B cells were treated with 0-50 μmol/L EGCG. Then the proliferation, apoptosis and migration of143B cells were measured by crystal violet staining, hoechst staining, cell wound-healing and Transwell chamber assays, respectively. The expression levels of apoptosis-and migrationrelated proteins were detected by Western blotting. The activity of Wnt/β-catenin signaling pathway was detected by luciferase reporter assay. Furthermore, the protein expression levels of β-catenin and its downstream target molecules c-Myc and cyclin D1 were detected by Western blotting. Results: After treatment with EGCG at highly concentration, the proliferation and migration of 143B cells were significantly inhibited (both P < 0.05), but the proportion of apoptotic cells was markedly increased (P < 0.05). Compared with the EGCG-untreated group, EGCG up-regulated the expressions of caspase-3 and its cleaved protein (both P < 0.05), and down-regulated the expressions of Bcl-2, matrix metalloproteinase-2 (MMP-2), β-catenin, c-Myc and cyclin D1 proteins (all P < 0.05). In addition, the luciferase activity reflecting Wnt/ β-catenin signaling pathway activity in EGCG-Treated group was significantly lower than that in EGCG-untreated group (P < 0.05). Conclusion: EGCG can inhibit the proliferation and migration of osteoscarcoma 143B cells, and promote apoptosis, which may be related to the blocking of Wnt/β-catenin signaling pathway.
