Prostaglandin E 2 promotes the nuclear accumulation of lymphoid enhancer factor-1 in poorly differentiated breast cancer cells

Ioannis Stasinopoulos, Tiffany Greenwood, Kristine Glunde, Zaver M. Bhujwalla

Research output: Contribution to journalArticlepeer-review

Abstract

Products of the COX reaction are frequently elevated in solid tumors and their roles in the malignant phenotype have been extensively investigated. We have shown that COX-2 is essential for the growth of MDA-MB-231 cells in the fat pad of SCID mice and for their extrapulmonary colonization following injection in the tail vein of SCID mice. The molecular changes that follow shRNA-mediated silencing of COX-2 include a significant downregulation of LEF-1, a transcription factor normally activated during development following the Wnt-induced nuclear translocation of β-catenin. We also report that COX-2-silenced cells have reduced nuclear accumulation of LEF-1 protein and that the COX-2 product PGE 2 partially restored nuclear LEF-1 expression in COX-2-silenced cells. Further, we demonstrate that, like parental COX-2 containing MDA-MB-231 cells, COX-2-silenced cells maintain nuclear localization of β-catenin.

Original languageEnglish (US)
Pages (from-to)9-14
Number of pages6
JournalProstaglandins and Other Lipid Mediators
Volume99
Issue number1-2
DOIs
StatePublished - Oct 2012

Keywords

  • Breast cancer
  • COX-2
  • Cyclooxygenase-2
  • Inflammation
  • LEF-1
  • Lymphoid enhancer factor-1
  • PGE
  • Prostaglandin E
  • Wnt
  • β-Catenin

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

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