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, Ta-Chien Tseng, Jen Hui Tsou, Ju-Ming Wang

Research output: Contribution to journalArticle

15 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

Fingerprint

Aurora Kinase C
CCAAT-Enhancer-Binding Proteins
Genomic Instability
Transcription
Tumor Necrosis Factor-alpha
Aneuploidy
Chromosomal Instability
Tissue
Inflammation
Centromere
Protein C
Carcinogenesis
Transcription Factors
Chemical activation
Growth
Research

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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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.",
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CCAAT/enhancer-binding protein δ mediates tumor necrosis factor α-induced aurora kinase C transcription and promotes genomic instability. / Wu, Sin Rong; Li, Chien Feng; Hung, Liang-Yi; Huang, A. Mei; Tseng, Ta-Chien; Tsou, Jen Hui; Wang, Ju-Ming.

In: Journal of Biological Chemistry, Vol. 286, No. 33, 19.08.2011, p. 28662-28670.

Research output: Contribution to journalArticle

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AU - Tseng, Ta-Chien

AU - Tsou, Jen Hui

AU - Wang, Ju-Ming

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