CCAAT/enhancer-binding protein δ mediates tumor necrosis factor α-induced aurora kinase C transcription and promotes genomic instability

Sin Rong Wu, Chien Feng Li, Liang Yi Hung, A. Mei Huang, Joseph T. Tseng, Jen Hui Tsou, Ju Ming Wang

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)

Abstract

Epidemiologic and clinical research indicates that chronic inflammation increases the risk of certain cancers, possibly through chromosomal instability. However, the mechanism of inflammation-dependent chromosomal instability associated with tumorigenesis is not well characterized. The transcription factor CCAAT/enhancer-binding protein δ (C/EBPδ, CEBPD) is induced by tumor necrosis factor α (TNFα) and expressed in chronically inflamed tissue. In this study, we show that TNFα promotes aneuploidy. Loss of CEBPD attenuated TNFα-induced aneuploidy, and CEBPD caused centromere abnormality. Additionally, TNFα-induced CEBPD expression augmented anchorage-independent growth. We found that TNFα induced expression of aurora kinase C (AURKC) through CEBPD, and that AURKC also causes aneuploidy. Furthermore, high CEBPD expression correlated with AURKC expression in inflamed cervical tissue specimens. These data provide insight into a novel function for CEBPD in inducing genomic instability through the activation of AURKC expression in response to inflammatory signals.

Original languageEnglish
Pages (from-to)28662-28670
Number of pages9
JournalJournal of Biological Chemistry
Volume286
Issue number33
DOIs
Publication statusPublished - 2011 Aug 19

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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