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

Research output: Contribution to journalArticle

67 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)95-100
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume302
Issue number1
DOIs
Publication statusPublished - Feb 28 2003

Fingerprint

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

Keywords

  • Angiogenesis
  • GL331
  • HIF-1α
  • HUVEC

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

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.

In: Biochemical and Biophysical Research Communications, Vol. 302, No. 1, 28.02.2003, p. 95-100.

Research output: Contribution to journalArticle

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, vol. 302, no. 1, pp. 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. In: Biochemical and Biophysical Research Communications. 2003 ; Vol. 302, No. 1. pp. 95-100.
@article{0815a94bf6d447169a8d2a978b1d9840,
title = "GL331 inhibits HIF-1α expression in a lung cancer model",
abstract = "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.",
keywords = "Angiogenesis, GL331, HIF-1α, HUVEC",
author = "Hang Chang and Kou-Gi Shyu and Lee, {Chun Chung} and Tsai, {Shiow Chwen} and Wang, {Bao Wei} and Lee, {Yu Hsien} and Shankung Lin",
year = "2003",
month = "2",
day = "28",
doi = "10.1016/S0006-291X(03)00111-6",
language = "English",
volume = "302",
pages = "95--100",
journal = "Biochemical and Biophysical Research Communications",
issn = "0006-291X",
publisher = "Elsevier B.V.",
number = "1",

}

TY - JOUR

T1 - GL331 inhibits HIF-1α expression in a lung cancer model

AU - Chang, Hang

AU - Shyu, Kou-Gi

AU - Lee, Chun Chung

AU - Tsai, Shiow Chwen

AU - Wang, Bao Wei

AU - Lee, Yu Hsien

AU - Lin, Shankung

PY - 2003/2/28

Y1 - 2003/2/28

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.

KW - Angiogenesis

KW - GL331

KW - HIF-1α

KW - HUVEC

UR - http://www.scopus.com/inward/record.url?scp=0037470368&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037470368&partnerID=8YFLogxK

U2 - 10.1016/S0006-291X(03)00111-6

DO - 10.1016/S0006-291X(03)00111-6

M3 - Article

C2 - 12593853

AN - SCOPUS:0037470368

VL - 302

SP - 95

EP - 100

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -