Regulation of anoikis by deleted in breast cancer-1 (DBC1) through NF-κB
作者： Sun Hee Park , Philip Riley , Steven M. Frisch
DOI: 10.1007/S10495-013-0847-1
关键词:
摘要: Anoikis-resistance of tumor cells is critical for anchorage-independent growth and metastasis. The inflammatory-response transcription factor NF-κB contributes to anoikis-resistance progression through mechanisms that are understood incompletely. Deleted in breast cancer-1 (DBC1) protein (KIAA1967) over-expressed several types, correlates with a poorer prognosis some cases. We report here DBC1 suppressed anoikis normal epithelial cancer cell lines. interacted IKK-β, stimulating its kinase activity, promoting transcriptional activity the phosphorylation relA serine-536 enhancing expression target genes, c-FLIP bcl-xl. Our results indicate an important co-factor control IKK-β-NF-κB signaling pathway regulates anoikis.
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