ATDC is required for the initiation of KRAS-induced pancreatic tumorigenesis

Lidong Wang, Huibin Yang, Andrea Zamperone, Daniel Diolaiti, Phillip L. Palmbos, Ethan V. Abel, Vinee Purohit, Igor Dolgalev, Andrew D. Rhim, Mats Ljungman, Christina H. Hadju, Christopher J. Halbrook, Dafna Bar-Sagi, Marina Pasca Di Magliano, Howard C. Crawford, Diane M. Simeone

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

Pancreatic adenocarcinoma (PDA) is an aggressive disease driven by oncogenic KRAS and characterized by late diagnosis and therapeutic resistance. Here we show that deletion of the ataxia-telangiectasia group D-comple-menting (Atdc) gene, whose human homolog is up-regulated in the majority of pancreatic adenocarcinoma, completely prevents PDA development in the context of oncogenic KRAS. ATDC is required for KRAS-driven ac-inar–ductal metaplasia (ADM) and its progression to pancreatic intraepithelial neoplasia (PanIN). As a result, mice lacking ATDC are protected from developing PDA. Mechanistically, we show ATDC promotes ADM progression to PanIN through activation of β-catenin signaling and subsequent SOX9 up-regulation. These results provide new insight into PDA initiation and reveal ATDC as a potential target for preventing early tumor-initiating events.

Original languageEnglish (US)
Pages (from-to)641-655
Number of pages15
JournalGenes and Development
Volume33
Issue number11-12
DOIs
StatePublished - Jun 1 2019

Keywords

  • ATDC
  • Acinar-to-ductal metaplasia
  • KRAS
  • PanIN lesion
  • Pancreatic ductal adenocarcinoma
  • SOX9
  • TRIM29
  • β-catenin]

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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