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Conditional ablation of C/EBP beta demonstrates its keratinocyte-specific requirement for cell survival and mouse skin tumorigenesis

  1. Author:
    Sterneck, E.
    Zhu, S.
    Ramirez, A.
    Jorcano, J. L.
    Smart, R. C.

  2. Author Address

    N Carolina State Univ, Dept Environm & Mol Toxicol, Cell Signaling & Canc Grp, Raleigh, NC 27695 USA. NCI, Mol Mech Dev Grp, Lab Prot Dynam & Signaling, Frederick, MD USA. CIEMAT, Repair & Tissue Engn Program, Madrid, Spain.;Smart, RC, N Carolina State Univ, Dept Environm & Mol Toxicol, Cell Signaling & Canc Grp, Raleigh, NC 27695 USA.;rcsmart@unity.ncsu.edu
    1. Year: 2006
    2. Date: Feb
  2. Journal: Oncogene
    1. 25
    2. 8
    3. Pages: 1272-1276
  4. Type of Article: Article
  5. ISSN: 0950-9232
  1. Abstract:

    The CCAAT/enhancer binding protein beta(C/EBP beta) is implicated in the regulation of many different molecular and physiological processes. Mice with a germline deletion of C/EBP beta (C/EBP beta(-/-)) display phenotypes in a multitude of cell types and organ systems, including skin where C/EBP beta(-/-) mice exhibit increased apoptosis in epidermal keratinocytes in response to carcinogen treatment and are completely resistant to carcinogen-induced skin tumorigenesis. To determine the contribution of systemic versus cell autonomous functions of C/EBP beta to specific phenotypes, mice with a conditional 'floxed' C/EBP beta null allele were generated. Epidermal-specific deletion of C/EBP beta was achieved by Cre recombinase expression from a keratin 5 (K5) promoter. Similar to C/EBP beta(-/-) mice, K5-Cre; C/EBP beta(fl)/(fl) mice were completely refractory to 7,12 dimethylbenz[a] anthracene (DMBA)-induced skin tumorigenesis and these mice displayed increased DMBA-induced apoptosis in epidermal keratinocytes compared to wild-type mice. In contrast, mice lacking the related gene, C/ EBP delta, were not resistant to DMBA-induced skin tumorigenesis, indicating a unique role of C/EBP beta in skin tumor development. Our findings demonstrate that C/EBP beta exerts an essential, keratinocyte-intrinsic role in cell survival in response to carcinogen treatment and the elimination of C/EBP beta in keratinocytes is sufficient to confer complete resistance of the skin to chemical carcinogenesis.

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External Sources

  1. View record in Web of Science®
  2. WOS: 000235537500014

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