Prkci Regulates Autophagy and Pancreatic Tumorigenesis in Mice

Kristin S. Inman, Yi Liu, Michele L. Scotti Buzhardt, Michael Leitges, Murli Krishna, Howard C. Crawford, Alan P. Fields, Nicole R. Murray

Research output: Contribution to journalArticlepeer-review


Protein kinase C iota (PKCι) functions as a bonafide human oncogene in lung and ovarian cancer and is required for KrasG12D-mediated lung cancer initiation and progression. PKCι expression is required for pancreatic cancer cell growth and maintenance of the transformed phenotype; however, nothing is known about the role of PKCι in pancreas development or pancreatic tumorigenesis. In this study, we investigated the effect of pancreas-specific ablation of PKCι expression on pancreatic cellular homeostasis, susceptibility to pancreatitis, and KrasG12D-mediated pancreatic cancer development. Knockout of pancreatic Prkci significantly increased pancreatic immune cell infiltration, acinar cell DNA damage, and apoptosis, but reduced sensitivity to caerulein-induced pancreatitis. Prkci-ablated pancreatic acinar cells exhibited P62 aggregation and a loss of autophagic vesicles. Loss of pancreatic Prkci promoted KrasG12D-mediated pancreatic intraepithelial neoplasia formation but blocked progression to adenocarcinoma, consistent with disruption of autophagy. Our results reveal a novel promotive role for PKCι in pancreatic epithelial cell autophagy and pancreatic cancer progression.

Original languageEnglish (US)
Article number796
Issue number3
StatePublished - Feb 1 2022


  • Autophagy
  • Immune cell infiltration
  • Pancreatic cancer
  • Protein kinase C iota
  • Tumor progression

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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