AI Article Synopsis
- PKCι is identified as an oncogene involved in lung and ovarian cancer, and is important for pancreatic cancer cell growth and maintenance.
- The study examines the effects of removing PKCι specifically in the pancreas, finding that this leads to increased immune cell infiltration, DNA damage, and cell death, while reducing the sensitivity to pancreatitis.
- Disrupting PKCι in pancreatic cells promotes early tumor formation but prevents further progression to a more aggressive cancer stage, highlighting its role in autophagy and cancer development.
Article Abstract
Protein kinase C iota (PKCι) functions as a bonafide human oncogene in lung and ovarian cancer and is required for -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 -mediated pancreatic cancer development. Knockout of pancreatic significantly increased pancreatic immune cell infiltration, acinar cell DNA damage, and apoptosis, but reduced sensitivity to caerulein-induced pancreatitis. -ablated pancreatic acinar cells exhibited P62 aggregation and a loss of autophagic vesicles. Loss of pancreatic promoted -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.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8834021 | PMC |
| http://dx.doi.org/10.3390/cancers14030796 | DOI Listing |
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