[Effect of EGCG on the proliferation and invasion of human hepatoma HepG2 cells].
Jingjing Cao, Hui Liang, Aiguo Ma, Ying Liu, Na Ge, Hongbin Yao
Abstract
Jingjing Cao, Hui Liang, Aiguo Ma, Ying Liu, Na Ge, Hongbin Yao
Abstract
OBJECTIVE: To investigate the effect and mechanism of EGCG on the proliferation and invasion of human hepatioma HepG2 cell. METHODS: Hepatioma HepG2 cell was treated with EGCG at different concentrations. The effect of EGCG on HepG2 proliferation was examined by CCK-8. The apoptosis of HepG2 treated with EGCG was observed by fluorescence microscopy and FCM via Annexin V-FITC/PI staining. The invasion of HepG2 was detected by Transwell assay. The expression of MMP-2 and VEGF was analyzed by ELISA. RESULTS: HepG2 proliferation was inhibited after treated with EGCG. The IC25 of 24 h and 48 h was 58.19 and 54.19 mg/L. The IC50 of 24 h and 48 h was 133.90 and 78.97 mg/L. The apoptosis of HepG2 was induced significantly after treated with 60 and 135 mg/L EGCG, and the number of cells crossing Matrigel membrane was (28.33+/-7.66) and 0 (P<0.05), and the inhibitory rate of invasion was 69.47% and 100%. The expression of MMP-2 and VEGF decreased significantly. CONCLUSION: EGCG suppressed the proliferation and invasion of HepG2 with the possible mechanism of inducing apoptosis and down-regulating the expression of MMP-2 and VEGF in HepG2.
OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE: To investigate the effect and mechanism of EGCG on the proliferation and invasion of human hepatioma HepG2 cell. METHODS: Hepatioma HepG2 cell was treated with EGCG at different concentrations. The effect of EGCG on HepG2 proliferation was examined by CCK-8. The apoptosis of HepG2 treated with EGCG was observed by fluorescence microscopy and FCM via Annexin V-FITC/PI staining. The invasion of HepG2 was detected by Transwell assay. The expression of MMP-2 and VEGF was analyzed by ELISA. RESULTS: HepG2 proliferation was inhibited after treated with EGCG. The IC25 of 24 h and 48 h was 58.19 and 54.19 mg/L. The IC50 of 24 h and 48 h was 133.90 and 78.97 mg/L. The apoptosis of HepG2 was induced significantly after treated with 60 and 135 mg/L EGCG, and the number of cells crossing Matrigel membrane was (28.33+/-7.66) and 0 (P<0.05), and the inhibitory rate of invasion was 69.47% and 100%. The expression of MMP-2 and VEGF decreased significantly. CONCLUSION: EGCG suppressed the proliferation and invasion of HepG2 with the possible mechanism of inducing apoptosis and down-regulating the expression of MMP-2 and VEGF in HepG2.
Key concepts: Apoptosis, Annexin, Matrigel, Cell growth, Chemistry, Molecular biology, Matrix metalloproteinase, Staining