The Effect of Epigallocatechin-3-gallate on HIF-1alpha and VEGF in Human Lung Cancer Cell Line.
10.4046/trd.2009.66.3.178
- Author:
Joo Han SONG
1
;
Eun Joo JEON
;
Hee Won KWAK
;
Hye Min LEE
;
Sung Gun CHO
;
Hyung Koo KANG
;
Sung Woon PARK
;
Jae Hee LEE
;
Byung Ook LEE
;
Jae Woo JUNG
;
Jae Cheol CHOI
;
Jong Wook SHIN
;
Ki Jeong KIM
;
Jae Yeol KIM
;
In Won PARK
;
Byoung Whui CHOI
Author Information
1. Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, Korea. iwpark@cau.ac.kr
- Publication Type:Original Article
- Keywords:
HIF-1alpha;
VEGF;
EGCG;
Lung cancer;
Hypoxia
- MeSH:
Actins;
Anoxia;
Carcinoma, Non-Small-Cell Lung;
Catechin;
Cell Culture Techniques;
Cell Cycle;
Cell Line;
Humans;
Lung;
Lung Neoplasms;
Neoplasm Metastasis;
Oxygen;
RNA, Messenger;
Tea;
Vascular Endothelial Growth Factor A
- From:Tuberculosis and Respiratory Diseases
2009;66(3):178-185
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Epigallocatechin-3-gallate (EGCG) is the major catechin in green tea, and has shown antiproliferative, antiangiogenic, antimetastatic and cell cycle pertubation activity in various tumor models. Hypoxia can be induced because angiogenesis is insufficient for highly proliferating cancer. Hypoxia-inducible factor-1alpha (HIF-1alpha) and its downstream target, vascular endothelial growth factor (VEGF), are important for angiogenesis, tumor growth and metastasis. The aim of this study was to determine how hypoxia could cause changes in the cellular phenomena and microenvironment in a non-small cell culture system and to examine the effects of EGCG on a HIF-1alpha and VEGF in A549 cell line. METHODS: A549 cells, a non-small cell lung cancer cell line, were cultured with DMEM and 10% fetal bovine serum. A decrease in oxygen tension was induced using a hypoxia microchamber and a CO2-N2 gas mixture. Gas analysis and a MTT assay were performed. The A549 cells were treated with EGCG (0, 12.5, 25, 50 micromol/L), and then examined by real-time-PCR analysis of HIF-1alpha, VEGF, and beta-actin mRNA. RESULTS: Hypoxia reduced the proliferation of A549 cells from normoxic conditions. EGCG inhibited HIF-1alpha transcription in A549 cells in a dose-dependent manner. Compared to HIF-1alpha, VEGF was not inhibited by EGCG. CONCLUSION: HIF-1alpha can be inhibited by EGCG. This suggests that targeting HIF-1alpha with a EGCG treatment may have therapeutic potential in non-small cell lung cancers.
