Abstract：
:The transcription factor nuclear factor-kappaB (NF-kappaB) is constitutively activated in many types of cancers and has been implicated in gene expression important for angiogenesis, tumor growth, progression, and metastasis. Here, we show that the NF-kappaB activator, IkappaB kinase-alpha (IKKalpha), but not IKKbeta, promotes endothelial cell motility and tumor angiogenesis. IKKalpha is elevated in tumor vasculature compared with normal endothelium. Overexpression of IKKalpha in endothelial cells promoted cell motility and vascular tubule formation in a three-dimensional culture assay, and conversely, knockdown of IKKalpha in endothelial cells inhibited cell motility, compared with controls. Interestingly, blocking NF-kappaB activation totally abolished IKKalpha-induced angiogenic function. Furthermore, using a tumor and endothelial cell cotransplantation model, we show that overexpression of IKKalpha in endothelial cells significantly increased tumor vascular formation compared with controls, which contributed to increased tumor growth and tumor cell proliferation, and decreased tumor cell apoptosis. Collectively, these findings have identified a new function for IKKalpha through the canonical NF-kappaB pathway in tumor angiogenesis.
journal_name
Cancer Resjournal_title
Cancer researchauthors
DeBusk LM,Massion PP,Lin PCdoi
10.1158/0008-5472.CAN-08-1833subject
Has Abstractpub_date
2008-12-15 00:00:00pages
10223-8issue
24eissn
0008-5472issn
1538-7445pii
68/24/10223journal_volume
68pub_type
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