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TNFalpha induces HIF-1alpha expression through activation of IKKbeta.

Abstract：

:The transcription factor hypoxia-inducible factor 1alpha (HIF-1alpha) is regulated by oxygen availability as well as various inflammatory mediators, including tumor necrosis factor alpha (TNFalpha). Early work suggested that the phosphatidylinositol-3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways are involved in TNFalpha-mediated HIF-1alpha accumulation and activation under normoxic conditions. Here, we provide evidence showing that IkappaB kinase beta (IKKbeta) is required for HIF-1alpha regulation by TNFalpha. We found that TNFalpha enhances HIF-1alpha protein expression in various breast cancer cell lines under either normoxic or hypoxia-mimicking conditions, but has little effect on the HIF-1alpha mRNA level. Increased HIF-1alpha expression was found in IKKbeta stable clones and transient transfectants, and depletion of IKKbeta consistently reduced the amount of HIF-1alpha protein. Treatment of cells with the IKKbeta inhibitor Bay 11-7082 reduced the TNFalpha-induced HIF-1alpha expression, suggesting that IKKbeta is required in this signaling pathway. Decreased expression of vascular endothelial growth factor (VEGF), a direct target of HIF-1alpha, was shown in IKKbeta-knockout mouse embryonic fibroblast cells. We further demonstrated a positive correlation between IKKbeta and VEGF expression in primary human breast cancer specimens. Our findings indicate that TNFalpha-induced HIF-1alpha accumulation is IKKbeta dependent, and may enable further understanding of the HIF-1alpha regulation by inflammatory signals.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Kuo HP,Lee DF,Xia W,Wei Y,Hung MC

doi

10.1016/j.bbrc.2009.09.042

subject

Has Abstract

pub_date

2009-11-27 00:00:00

pages

640-4

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(09)01844-0

journal_volume

389

pub_type

杂志文章

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