Abstract：
:Triple-negative breast cancers (TNBC), which include the basal-like and claudin-low disease subtypes, are aggressive malignancies for which effective therapeutic targets are lacking. NF-κB activation has an established role in breast malignancy, and it is higher in TNBC than other breast cancer subtypes. On this basis, we hypothesized that proteins derived from NF-κB target genes might be molecular targets for TNBC therapy. In this study, we conducted a microarray-based screen for novel NF-κB-inducible proteins as candidate therapeutic targets, identifying tropomodulin 1 (TMOD1) as a lead candidate. TMOD1 expression was regulated directly by NF-κB and was significantly higher in TNBC than other breast cancer subtypes. TMOD1 elevation is associated with enhanced tumor growth in a mouse tumor xenograft model and in a 3D type I collagen culture. TMOD1-dependent tumor growth was correlated with MMP13 induction, which was mediated by TMOD1-dependent accumulation of β-catenin. Overall, our study highlighted a novel TMOD1-mediated link between NF-κB activation and MMP13 induction, which accounts in part for the NF-κB-dependent malignant phenotype of TNBC.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Ito-Kureha T,Koshikawa N,Yamamoto M,Semba K,Yamaguchi N,Yamamoto T,Seiki M,Inoue Jdoi
10.1158/0008-5472.CAN-13-3455subject
Has Abstractpub_date
2015-01-01 00:00:00pages
62-72issue
1eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-13-3455journal_volume
75pub_type
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