PUBLICATION

Genome-wide Profiling of AP-1–Regulated Transcription Provides Insights into the Invasiveness of Triple-Negative Breast Cancer

Authors
Zhao, C., Qiao, Y., Jonsson, P., Wang, J., Xu, L., Rouhi, P., Sinha, I., Cao, Y., Williams, C., Dahlman-Wright, K.
ID
ZDB-PUB-140517-9
Date
2014
Source
Cancer research   74(14): 3983-94 (Journal)
Registered Authors
Sinha, Indranil
Keywords
none
MeSH Terms
  • Cadherins/metabolism
  • Cell Line, Tumor
  • Cell Proliferation
  • Female
  • Gene Expression Profiling*
  • Gene Expression Regulation, Neoplastic*
  • Gene Knockdown Techniques
  • Homeodomain Proteins/metabolism
  • Humans
  • MAP Kinase Signaling System
  • Models, Biological
  • Neoplasm Invasiveness
  • Neoplasms, Basal Cell
  • Phosphatidylinositol 3-Kinases/metabolism
  • Prognosis
  • Proto-Oncogene Proteins c-akt/metabolism
  • Proto-Oncogene Proteins c-fos/genetics
  • Proto-Oncogene Proteins c-fos/metabolism
  • Proto-Oncogene Proteins c-jun/genetics
  • Proto-Oncogene Proteins c-jun/metabolism
  • Repressor Proteins/metabolism
  • Transcription Factor AP-1/genetics
  • Transcription Factor AP-1/metabolism*
  • Transcription, Genetic*
  • Transcriptome
  • Triple Negative Breast Neoplasms/genetics*
  • Triple Negative Breast Neoplasms/metabolism*
  • Triple Negative Breast Neoplasms/mortality
  • Triple Negative Breast Neoplasms/pathology
PubMed
24830720 Full text @ Cancer Res.
Abstract
Triple-negative breast cancer (TNBC) is an aggressive clinical subtype accounting for up to 20% of all breast cancers, but its malignant determinants remain largely undefined. Here we show that in TNBC the overexpression of Fra-1, a component of the transcription factor AP-1, offers prognostic potential. Fra-1 depletion or its heterodimeric partner c-Jun inhibits the proliferative and invasive phenotypes of TNBC cells in vitro. Similarly, RNAi-mediated attenuation of Fra-1 or c-Jun reduced cellular invasion in vivo in a zebrafish tumor xenograft model. Exploring the AP-1 cistrome and the AP-1-regulated transcriptome, we obtained insights into the transcriptional regulatory networks of AP-1 in TNBC cells. Among the direct targets identified for Fra-1/c-Jun involved in proliferation, adhesion and cell-cell contact, we found that AP-1 repressed expression of E-cadherin by transcriptional upregulation of ZEB2 to stimulate cell invasion. Overall, this work illuminates the pathways through which TNBC cells acquire invasive and proliferative properties.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping