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

Lidong Wang1,2, Huibin Yang3, Andrea Zamperone1,2

  • 1Department of Surgery, New York University School of Medicine, New York, New York 10016, USA.

Genes & Development
|May 4, 2019
PubMed

Insights

Deleting the ataxia-telangiectasia group D-complementing (ATDC) gene prevents pancreatic adenocarcinoma (PDA) development. ATDC is crucial for KRAS-driven precancerous lesion progression in the pancreas.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Pancreatic adenocarcinoma (PDA) is a lethal malignancy often diagnosed late.
  • Oncogenic KRAS mutations drive PDA, contributing to therapeutic resistance.
  • The ataxia-telangiectasia group D-complementing (ATDC) gene's human homolog is upregulated in most PDA cases.

Purpose of the Study:

  • To investigate the role of ATDC in pancreatic cancer initiation and progression.
  • To determine if ATDC is essential for KRAS-driven pancreatic adenocarcinoma development.

Main Methods:

  • Utilized a mouse model with oncogenic KRAS and ATDC gene deletion.
  • Analyzed the impact of ATDC absence on acinar-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN) formation.
  • Investigated the molecular mechanisms involving beta-catenin signaling and SOX9.

Main Results:

  • Complete prevention of PDA development in mice lacking the ATDC gene.
  • ATDC is essential for KRAS-driven ADM and its progression to PanIN.
  • ATDC promotes ADM to PanIN transition via beta-catenin/SOX9 pathway activation.

Conclusions:

  • ATDC plays a critical role in the initiation of pancreatic adenocarcinoma.
  • Targeting ATDC may offer a strategy to prevent early pancreatic tumor development.
  • Understanding ATDC's function provides new insights into PDA pathogenesis.
Keywords:
SOX9ATDCKRASPanIN lesionTRIM29acinar-to-ductal metaplasiapancreatic ductal adenocarcinomaβ-catenin

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