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The Ets dominant repressor En/Erm enhances intestinal epithelial tumorigenesis in ApcMin mice.

AbstractBACKGROUND:
Ets transcription factors have been widely implicated in the control of tumorigenesis, with most studies suggesting tumor-promoting roles. However, few studies have examined Ets tumorigenesis-modifying functions in vivo using model genetic systems.
METHODS:
Using mice expressing a previously characterized Ets dominant repressor transgene in the intestinal epithelium (Villin-En/Erm), we examined the consequences of blocking endogenous Ets-mediated transcriptional activation on tumorigenesis in the ApcMin model of intestinal carcinoma.
RESULTS:
En/Erm expression in the intestine, at levels not associated with overt crypt-villus dysmorphogenesis, results in a marked increase in tumor number in ApcMin animals. Moreover, when examined histologically, tumors from En/Erm-expressing animals show a trend toward greater stromal invasiveness. Detailed analysis of crypt-villus homeostasis in these En/Erm transgenic animals suggests increased epithelial turnover as one possible mechanism for the enhanced tumorigenesis.
CONCLUSION:
Our findings provide in vivo evidence for a tumor-restricting function of endogenous Ets factors in the intestinal epithelium.
AuthorsPaul Jedlicka, Xiaomei Sui, Arthur Gutierrez-Hartmann
JournalBMC cancer (BMC Cancer) Vol. 9 Pg. 197 (Jun 22 2009) ISSN: 1471-2407 [Electronic] England
PMID19545444 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • DNA-Binding Proteins
  • Etv5 protein, mouse
  • Proto-Oncogene Proteins c-ets
  • Transcription Factors
Topics
  • Animals
  • Carcinoma (genetics)
  • DNA-Binding Proteins (genetics, physiology)
  • Gene Expression Regulation, Neoplastic
  • Genes, Dominant
  • Immunohistochemistry
  • Intestinal Neoplasms (genetics)
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Models, Biological
  • Models, Genetic
  • Neoplasm Invasiveness
  • Proto-Oncogene Proteins c-ets (genetics, physiology)
  • Transcription Factors (genetics, physiology)
  • Transgenes

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