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KMID : 0383820090660030178
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Tuberculosis and Respiratory Diseases
2009 Volume.66 No. 3 p.178 ~ p.185
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The Effect of Epigallocatechin-3-gallate on HIF-1α and VEGF in Human Lung Cancer Cell Line
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Song Ju-Han
Jung Jae-Woo
Jeon Eun-Ju
Choi Jae-Cheol
Shin Jong-Wook
Kim Jae-Yeol
Park In-Won
Choi Byoung-Whui
Kwak Hee-Won
Kim Ki-Jeong
Kang Hyung-Gu
Lee Hye-Min
Cho Sung-Keun
Park Sung-Woon
Lee Jae-Hee
Lee Byung-Ook
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Abstract
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Background:Epigallocatechin-3-gallate (EGCG) is the major catechin in green tea, and has shown ntiproliferative, 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-1α (HIF-1α) 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-1α 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 μmol/L), and then examined by real-time-PCR analysis of HIF-1α, VEGF, and β-actin mRNA.
Results:Hypoxia reduced the proliferation of A549 cells from normoxic conditions. EGCG inhibited HIF-1α transcription in A549 cells in a dose-dependent manner. Compared to HIF-1α, VEGF was not inhibited by EGCG.
Conclusion:HIF-1α can be inhibited by EGCG. This suggests that targeting HIF-1α with a EGCG treatment may have therapeutic potential in non-small cell lung cancers.
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KEYWORD
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HIF-1α, VEGF, EGCG, Lung cancer, Hypoxia
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