GL331 inhibits HIF-1α expression in a lung cancer model

Hang Chang, Kou-Gi Shyu, Chun Chung Lee, Shiow Chwen Tsai, Bao Wei Wang, Yu Hsien Lee, Shankung Lin

研究成果: 雜誌貢獻文章

67 引文 (Scopus)

摘要

We have studied GL331's anti-cancer mechanisms by studying their effect on the tumor-induced angiogenesis. Human lung adenocarcinoma CL1-5 cells were treated with GL331 and then maintained in serum-reduced, GL331-free medium for the preparation of condition mediums. These condition mediums were tested for their capability to induce in vitro angiogenesis, i.e., HUVEC tube formation and migration. We found that mediums generated from GL331-treated CL1-5 cells presented reduced ability of inducing in vitro angiogenesis. Western blot analyses showed that both VEGF and HIF-1α were down-regulated in GL331-treated CL1-5 cells. Northern blot and EMSA analyses showed that GL331 down-regulated HIF-1α expression without decreasing the stability of HIF-1α mRNA, and that GL331 decreased the binding of CL1-5-derived nuclear components to the promoter of HIF-1α gene. Therefore, our data showed that GL331 is a potent inhibitor of tumor-induced angiogenesis. The underlying mechanisms might involve at least the inhibition of HIF-1α expression, probably through transcriptional repression.
原文英語
頁(從 - 到)95-100
頁數6
期刊Biochemical and Biophysical Research Communications
302
發行號1
DOIs
出版狀態已發佈 - 二月 28 2003

指紋

Lung Neoplasms
Tumors
Neoplasms
GL 331
Northern Blotting
Vascular Endothelial Growth Factor A
Genes
Western Blotting
Messenger RNA
Serum

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

引用此文

Chang, H., Shyu, K-G., Lee, C. C., Tsai, S. C., Wang, B. W., Lee, Y. H., & Lin, S. (2003). GL331 inhibits HIF-1α expression in a lung cancer model. Biochemical and Biophysical Research Communications, 302(1), 95-100. https://doi.org/10.1016/S0006-291X(03)00111-6

GL331 inhibits HIF-1α expression in a lung cancer model. / Chang, Hang; Shyu, Kou-Gi; Lee, Chun Chung; Tsai, Shiow Chwen; Wang, Bao Wei; Lee, Yu Hsien; Lin, Shankung.

於: Biochemical and Biophysical Research Communications, 卷 302, 編號 1, 28.02.2003, p. 95-100.

研究成果: 雜誌貢獻文章

Chang, H, Shyu, K-G, Lee, CC, Tsai, SC, Wang, BW, Lee, YH & Lin, S 2003, 'GL331 inhibits HIF-1α expression in a lung cancer model', Biochemical and Biophysical Research Communications, 卷 302, 編號 1, 頁 95-100. https://doi.org/10.1016/S0006-291X(03)00111-6
Chang, Hang ; Shyu, Kou-Gi ; Lee, Chun Chung ; Tsai, Shiow Chwen ; Wang, Bao Wei ; Lee, Yu Hsien ; Lin, Shankung. / GL331 inhibits HIF-1α expression in a lung cancer model. 於: Biochemical and Biophysical Research Communications. 2003 ; 卷 302, 編號 1. 頁 95-100.
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AU - Lin, Shankung

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N2 - We have studied GL331's anti-cancer mechanisms by studying their effect on the tumor-induced angiogenesis. Human lung adenocarcinoma CL1-5 cells were treated with GL331 and then maintained in serum-reduced, GL331-free medium for the preparation of condition mediums. These condition mediums were tested for their capability to induce in vitro angiogenesis, i.e., HUVEC tube formation and migration. We found that mediums generated from GL331-treated CL1-5 cells presented reduced ability of inducing in vitro angiogenesis. Western blot analyses showed that both VEGF and HIF-1α were down-regulated in GL331-treated CL1-5 cells. Northern blot and EMSA analyses showed that GL331 down-regulated HIF-1α expression without decreasing the stability of HIF-1α mRNA, and that GL331 decreased the binding of CL1-5-derived nuclear components to the promoter of HIF-1α gene. Therefore, our data showed that GL331 is a potent inhibitor of tumor-induced angiogenesis. The underlying mechanisms might involve at least the inhibition of HIF-1α expression, probably through transcriptional repression.

AB - We have studied GL331's anti-cancer mechanisms by studying their effect on the tumor-induced angiogenesis. Human lung adenocarcinoma CL1-5 cells were treated with GL331 and then maintained in serum-reduced, GL331-free medium for the preparation of condition mediums. These condition mediums were tested for their capability to induce in vitro angiogenesis, i.e., HUVEC tube formation and migration. We found that mediums generated from GL331-treated CL1-5 cells presented reduced ability of inducing in vitro angiogenesis. Western blot analyses showed that both VEGF and HIF-1α were down-regulated in GL331-treated CL1-5 cells. Northern blot and EMSA analyses showed that GL331 down-regulated HIF-1α expression without decreasing the stability of HIF-1α mRNA, and that GL331 decreased the binding of CL1-5-derived nuclear components to the promoter of HIF-1α gene. Therefore, our data showed that GL331 is a potent inhibitor of tumor-induced angiogenesis. The underlying mechanisms might involve at least the inhibition of HIF-1α expression, probably through transcriptional repression.

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