Hypoxia-Inducible Factor-1α Downregulation by Small Interfering RNA Inhibits Proliferation, Induces Apoptosis, and Enhances Radiosensitivity in Chemical Hypoxic Human Hepatoma SMMC-7721 Cells

2011 ◽  
Vol 26 (5) ◽  
pp. 565-571 ◽  
Author(s):  
Wei Yang ◽  
Ting Sun ◽  
Jianping Cao ◽  
Saijun Fan
Keyword(s):  
Small Interfering Rna ◽  
Hypoxia Inducible Factor ◽  
Human Hepatoma ◽  
Hypoxia Inducible Factor 1Α ◽  
Interfering Rna

Effect of Small Interfering RNA Targeting Hypoxia-inducible Factor-1α on Radiosensitivity of PC3 Cell Line

Urology ◽  
2012 ◽  
Vol 79 (3) ◽  
pp. 744.e17-744.e24 ◽  
Author(s):  
Yuhua Huang ◽  
Jiang Yu ◽  
Chunyin Yan ◽  
Jianquan Hou ◽  
Jingxian Pu ◽  
...  
Keyword(s):  
Cell Line ◽  
Small Interfering Rna ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α ◽  
Rna Targeting ◽  
Pc3 Cell Line ◽  
Interfering Rna

Enhanced Sensitivity of Human Hepatoma Cells to 5-Fluorouracil by Small Interfering RNA Targeting Bcl-2

2005 ◽  
Vol 24 (12) ◽  
pp. 805-809 ◽  
Author(s):  
Tatsuo Kanda ◽  
Osamu Yokosuka ◽  
Fumio Imazeki ◽  
Makoto Arai ◽  
Hiromitsu Saisho
Keyword(s):  
Small Interfering Rna ◽  
Hepatoma Cells ◽  
Human Hepatoma ◽  
Human Hepatoma Cells ◽  
Enhanced Sensitivity ◽  
Rna Targeting ◽  
Interfering Rna

scholarly journals Hypoxia-Induced Autophagy Is Mediated through Hypoxia-Inducible Factor Induction of BNIP3 and BNIP3L via Their BH3 Domains

2009 ◽  
Vol 29 (10) ◽  
pp. 2570-2581 ◽  
Author(s):  
Grégory Bellot ◽  
Raquel Garcia-Medina ◽  
Pierre Gounon ◽  
Johanna Chiche ◽  
Danièle Roux ◽  
...  
Keyword(s):  
Cell Death ◽  
Tumor Progression ◽  
Cell Survival ◽  
Small Interfering Rna ◽  
Hypoxia Inducible Factor ◽  
Ectopic Expression ◽  
Survival Mechanism ◽  
Hypoxic Conditions ◽  
Interfering Rna

ABSTRACT While hypoxia-inducible factor (HIF) is a major actor in the cell survival response to hypoxia, HIF also is associated with cell death. Several studies implicate the HIF-induced putative BH3-only proapoptotic genes bnip3 and bnip3l in hypoxia-mediated cell death. We, like others, do not support this assertion. Here, we clearly demonstrate that the hypoxic microenvironment contributes to survival rather than cell death by inducing autophagy. The ablation of Beclin1, a major actor of autophagy, enhances cell death under hypoxic conditions. In addition, the ablation of BNIP3 and/or BNIP3L triggers cell death, and BNIP3 and BNIP3L are crucial for hypoxia-induced autophagy. First, while the small interfering RNA-mediated ablation of either BNIP3 or BNIP3L has little effect on autophagy, the combined silencing of these two HIF targets suppresses hypoxia-mediated autophagy. Second, the ectopic expression of both BNIP3 and BNIP3L in normoxia activates autophagy. Third, 20-mer BH3 peptides of BNIP3 or BNIP3L are sufficient in initiating autophagy in normoxia. Herein, we propose a model in which the atypical BH3 domains of hypoxia-induced BNIP3/BNIP3L have been designed to induce autophagy by disrupting the Bcl-2-Beclin1 complex without inducing cell death. Hypoxia-induced autophagy via BNIP3 and BNIP3L is clearly a survival mechanism that promotes tumor progression.

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