ATDC/TRIM29 phosphorylation by ATM/MAPKAP kinase 2 mediates radioresistance in pancreatic cancer cells.

نویسندگان

  • Lidong Wang
  • Huibin Yang
  • Phillip L Palmbos
  • Gina Ney
  • Taylor Ann Detzler
  • Dawn Coleman
  • Jacob Leflein
  • Mary Davis
  • Min Zhang
  • Wenhua Tang
  • J Kevin Hicks
  • Corey M Helchowski
  • Jayendra Prasad
  • Theodore S Lawrence
  • Liang Xu
  • Xiaochun Yu
  • Christine E Canman
  • Mats Ljungman
  • Diane M Simeone
چکیده

Pancreatic ductal adenocarcinoma (PDAC) is characterized by therapeutic resistance for which the basis is poorly understood. Here, we report that the DNA and p53-binding protein ATDC/TRIM29, which is highly expressed in PDAC, plays a critical role in DNA damage signaling and radioresistance in pancreatic cancer cells. Ataxia-telangiectasia group D-associated gene (ATDC) mediated resistance to ionizing radiation in vitro and in vivo in mouse xenograft assays. ATDC was phosphorylated directly by MAPKAP kinase 2 (MK2) at Ser550 in an ATM-dependent manner. Phosphorylation at Ser-550 by MK2 was required for the radioprotective function of ATDC. Our results identify a DNA repair pathway leading from MK2 and ATM to ATDC, suggesting its candidacy as a therapeutic target to radiosensitize PDAC and improve the efficacy of DNA-damaging treatment.

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عنوان ژورنال:
  • Cancer research

دوره 74 6  شماره 

صفحات  -

تاریخ انتشار 2014