Regulation of anoikis by deleted in breast cancer-1 (DBC1) through NF-κB

被引：48

作者：

Park, Sun Hee ^{[1
]}

Riley, Philip ^{[1
]}

Frisch, Steven M. ^{[1
,2
]}

机构：

[1] W Virginia Univ, Mary Babb Randolph Canc Ctr, Morgantown, WV 26506 USA

[2] W Virginia Univ, Dept Biochem, Morgantown, WV 26506 USA

来源：

APOPTOSIS | 2013年 / 18卷 / 08期

关键词：

Anoikis; DBC1; NF-kappa B; IKK-beta; INTESTINAL EPITHELIAL-CELLS; NUCLEAR IKK-BETA; NEGATIVE REGULATOR; SIRT1; DEACETYLASE; PROTEIN; ALPHA; PHOSPHORYLATION; ACTIVATION; RESISTANCE; EXPRESSION;

D O I：

10.1007/s10495-013-0847-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Anoikis-resistance of tumor cells is critical for anchorage-independent growth and metastasis. The inflammatory-response transcription factor NF-kappa B contributes to anoikis-resistance and tumor progression through mechanisms that are understood incompletely. Deleted in breast cancer-1 (DBC1) protein (KIAA1967) is over-expressed in several tumor types, and correlates with a poorer prognosis in some cases. We report here that DBC1 suppressed anoikis in normal epithelial and breast cancer cell lines. DBC1 interacted with IKK-beta, stimulating its kinase activity, promoting NF-kappa B transcriptional activity through the phosphorylation of relA serine-536 and enhancing the expression of the NF-kappa B target genes, c-FLIP and bcl-xl. Our results indicate that DBC1 is an important co-factor for the control of the IKK-beta-NF-kappa B signaling pathway that regulates anoikis.

引用

页码：949 / 962

页数：14

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