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ERalpha-induced C/EBPD inhibits SNAI2 expression and is a marker of good prognosis in breast cancer

Thursday, September 17, 2015 — Poster Session II

12:00 p.m. – 1:30 p.m.
FAES Terrace


  • D Mendoza-Villanueva
  • K Balamurugan
  • R Ali
  • SR Kim
  • S Sharan
  • R Johnson
  • A Merchant
  • C Caldas
  • G Landberg
  • E Sterneck


Inflammation and hypoxia are strongly linked to cancer progression. Hypoxia and inflammatory cytokines like IL-6 signal in part through the transcription factor C/EBPD, which drives mesenchymal features and malignant progression of glioblastoma. Here we report a different role for C/EBPD in breast cancer. Previous studies in MMTV-Neu transgenic mice revealed contrasting functions of C/EBPD in reducing mammary tumor multiplicity while promoting metastasis. This study shows that the C/EBPD protein is expressed in normal breast and low-grade oestrogen receptor positive (ER+) cancers, and correlates with longer progressionfree survival of breast cancer patients. Functional studies in cell lines show that ERα promotes C/EBPD protein stability, and that C/EBPD attenuates cell growth, motility and invasiveness by inhibiting expression of the SNAI2 (Slug) transcriptional repressor, leading to expression of CDKN1A (p21CIP1/WAF1). Expression of CEBPD but not CEBPB mRNA in combination with IL6 correlates with lower risk of progression in ER+ breast cancer patients. These findings indicate that C/EBPD attenuates progression of ER+ breast cancer and support a potentially beneficial role for the IL-6 pathway in ER+ breast cancer.

Category: Cancer Biology