Oncogenic Function of ATDC in Pancreatic Cancer through Wnt Pathway Activation and β-Catenin Stabilization

Lidong Wang, David G. Heidt, Cheong J. Lee, Huibin Yang, Craig D. Logsdon, Lizhi Zhang, Eric R. Fearon, Mats Ljungman, Diane M. Simeone

Research output: Contribution to journalArticle

152 Scopus citations

Abstract

Pancreatic cancer is a deadly disease characterized by late diagnosis and resistance to therapy. Much progress has been made in defining gene defects in pancreatic cancer, but a full accounting of its molecular pathogenesis remains to be provided. Here, we show that expression of the ataxia-telangiectasia group D complementing gene (ATDC), also called TRIM29, is elevated in most invasive pancreatic cancers and pancreatic cancer precursor lesions. ATDC promoted cancer cell proliferation in vitro and enhanced tumor growth and metastasis in vivo. ATDC expression correlated with elevated β-catenin levels in pancreatic cancer, and β-catenin function was required for ATDC's oncogenic effects. ATDC was found to stabilize β-catenin via ATDC-induced effects on the Disheveled-2 protein, a negative regulator of glycogen synthase kinase 3β in the Wnt/β-catenin signaling pathway.

Original languageEnglish (US)
Pages (from-to)207-219
Number of pages13
JournalCancer cell
Volume15
Issue number3
DOIs
StatePublished - Mar 3 2009

Keywords

  • CELLCYCLE
  • SIGNALING

ASJC Scopus subject areas

  • Oncology
  • Cell Biology
  • Cancer Research

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    Wang, L., Heidt, D. G., Lee, C. J., Yang, H., Logsdon, C. D., Zhang, L., Fearon, E. R., Ljungman, M., & Simeone, D. M. (2009). Oncogenic Function of ATDC in Pancreatic Cancer through Wnt Pathway Activation and β-Catenin Stabilization. Cancer cell, 15(3), 207-219. https://doi.org/10.1016/j.ccr.2009.01.018