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Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer

Author

Listed:
  • Ligia I. Bastea

    (Mayo Clinic)

  • Xiang Liu

    (Mayo Clinic
    University of Nebraska Medical Center)

  • Alicia K. Fleming

    (Mayo Clinic)

  • Veethika Pandey

    (Mayo Clinic)

  • Heike Döppler

    (Mayo Clinic)

  • Brandy H. Edenfield

    (Mayo Clinic)

  • Murli Krishna

    (Mayo Clinic)

  • Lizhi Zhang

    (Mayo Clinic)

  • E. Aubrey Thompson

    (Mayo Clinic)

  • Paul M. Grandgenett

    (University of Nebraska Medical Center)

  • Michael A. Hollingsworth

    (University of Nebraska Medical Center)

  • DeLisa Fairweather

    (Mayo Clinic)

  • Dahn Clemens

    (University of Nebraska Medical Center)

  • Peter Storz

    (Mayo Clinic)

Abstract

The development of pancreatic cancer requires both, acquisition of an oncogenic mutation in KRAS as well as an inflammatory insult. However, the physiological causes for pancreatic inflammation are less defined. We show here that oncogenic KRas-expressing pre-neoplastic lesion cells upregulate coxsackievirus (CVB) and adenovirus receptor (CAR). This facilitates infections from enteroviruses such as CVB3, which can be detected in approximately 50% of pancreatic cancer patients. Moreover, using an animal model we show that a one-time pancreatic infection with CVB3 in control mice is transient, but in the presence of oncogenic KRas drives chronic inflammation and rapid development of pancreatic cancer. We further demonstrate that a knockout of CAR in pancreatic lesion cells blocks these CVB3-induced effects. Our data demonstrate that KRas-caused lesions promote the development of pancreatic cancer by enabling certain viral infections.

Suggested Citation

  • Ligia I. Bastea & Xiang Liu & Alicia K. Fleming & Veethika Pandey & Heike Döppler & Brandy H. Edenfield & Murli Krishna & Lizhi Zhang & E. Aubrey Thompson & Paul M. Grandgenett & Michael A. Hollingswo, 2024. "Coxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer," Nature Communications, Nature, vol. 15(1), pages 1-11, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-55043-x
    DOI: 10.1038/s41467-024-55043-x
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    as
    1. Geou-Yarh Liou & Heike Döppler & Ursula B. Braun & Richard Panayiotou & Michele Scotti Buzhardt & Derek C. Radisky & Howard C. Crawford & Alan P. Fields & Nicole R. Murray & Q. Jane Wang & Michael Lei, 2015. "Protein kinase D1 drives pancreatic acinar cell reprogramming and progression to intraepithelial neoplasia," Nature Communications, Nature, vol. 6(1), pages 1-11, May.
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