비소세포폐암주에서 저산소상태에 의해 유발된 HIFa-1α와 VEGF의 발현증가에 미치는 Epigallocatechin-3-gallate의 억제 효과

초록

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-1α (HIF-lα) 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-1 α 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-N 2 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-1 α, VEGF, and β-actin mRNA. Results: Hypoxia reduced the proliferation of A549 cells from normoxic conditions. EGCG inhibited HIF-1 α transcription in A549 cells in a dose-dependent manner. Compared to HIF-1α, VEGF was not inhibited by EGCG. Conclusion: HIF-1 α can be inhibited by EGCG. This suggests that targeting HIF-1 α with a EGCG treatment may- have therapeutic potential in non-small cell lung cancers. Copyright © 2009. The Korean Academy of Tuberculosis and Respiratory Diseases. All rights reserved.

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