Inhibitory Effect of EGCG on angiogenesis induced by multiple myeloma cell line KM3 and its mechanism.
- Author:
Jing SHAO
1
;
Zhi-Chao CHEN
;
Qiu-Bai LI
;
Jian LÜ
Author Information
1. Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
Angiogenesis Inhibitors;
pharmacology;
Catechin;
analogs & derivatives;
pharmacology;
Cell Line, Tumor;
Down-Regulation;
Humans;
Multiple Myeloma;
blood supply;
metabolism;
RNA, Messenger;
metabolism;
Vascular Endothelial Growth Factor A;
metabolism
- From:
Journal of Experimental Hematology
2007;15(5):973-977
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the effect of [(-)-epigallocatechin-3-gallate (EGCG)] on angiogenesis induced by multiple myeloma cell line KM3 and its mechanism. The effects of KM3 cell supernatant after being treated with EGCG in different concentrations on migration and vascular formation ability of endothelial cell line HUVEC were investigated through culture of MM cell line KM3 in vitro. The secretion level of vascular endothelial growth factor (VEGF) in KM3 cell supernatant and the expression level of VEGF mRNA in KM3 were detected by ELISA and RT-PCR respectively. The results indicated that the KM3 cell supernatant significantly induced endothelial cell migration and vascular formation in vitro. EGCG inhibited the effect of endothelial cell migration induced by KM3 cell supernatant, and the numbers of migrated cells were 414 +/- 27, 299 +/- 70, 202 +/- 42 and 116 +/- 13 at 5, 25, 50, 100 micromol/L respectively. The numbers of migrated cells showed negative correlation with the dose of EGCG (r = -0.952, p < 0.05). The areas of the capillary-like structures decreased while the concentrations of EGCG increased, 88343.9 +/- 3231.1 microm(2) at 25 micromol/L, 60897.5 +/- 914.1 microm2 at 50 micromol/L, which were significantly less than that in the control (p < 0.01) and showed negative correlation with the dose of EGCG (r = -0.888, p < 0.05). 48 hours after treatment with EGCG at concentrations of 5, 25, 50 and 100 micromol/L, the levels of VEGF in the culture supernatant were 1399.0 +/- 47.4, 660.1 +/- 5.7, 108.5 +/- 5.8 and 26.2 +/- 18.6 pg/ml respectively. Except 5 micromol/L, all the other groups showed significant changes while compared with the controls (p < 0.01). Furthermore, EGCG depressed the mRNA expression of VEGF in KM3 cells in a dose-dependent manner. It is concluded that the EGCG can significantly inhibit angiogenic ability of multiple myeloma KM3 cells, its pharmacological mechanism may be downregulation of VEGF mRNA expression and reduction of VEGF secretion.
