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

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. Hollingsworth, DeLisa Fairweather, Dahn Clemens and Peter Storz ()
Additional contact information
Ligia I. Bastea: Mayo Clinic
Xiang Liu: Mayo Clinic
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

Nature Communications, 2024, vol. 15, issue 1, 1-11

Abstract: 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.

Date: 2024
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DOI: 10.1038/s41467-024-55043-x

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