| First Author | Roy RV | Year | 2023 |
| Journal | Cancer Lett | Volume | 578 |
| Pages | 216455 | PubMed ID | 37865160 |
| Mgi Jnum | J:344342 | Mgi Id | MGI:7546623 |
| Doi | 10.1016/j.canlet.2023.216455 | Citation | Roy RV, et al. (2023) Pancreatic Ubap2 deletion regulates glucose tolerance, inflammation, and protection from cerulein-induced pancreatitis. Cancer Lett 578:216455 |
| abstractText | Ubiquitin-binding associated protein 2 (UBAP2) is reported to promote macropinocytosis and pancreatic adenocarcinoma (PDAC) growth, however, its role in normal pancreatic function remains unknown. We addressed this knowledge gap by generating UBAP2 knockout (U2KO) mice under a pancreas-specific Cre recombinase (Pdx1-Cre). Pancreatic architecture remained intact in U2KO animals, but they demonstrated slight glucose intolerance compared to controls. Upon cerulein challenge to induce pancreatitis, U2KO animals had reduced levels of several pancreatitis-relevant cytokines, amylase and lipase in the serum, reduced tissue damage, and lessened neutrophil infiltration into the pancreatic tissue. Mechanistically, cerulein-challenged U2KO animals revealed reduced NF-kappaB activation compared to controls. In vitro promoter binding studies confirmed the reduction of NF-kappaB binding to its target molecules supporting UBAP2 as a new regulator of inflammation in pancreatitis and may be exploited as a therapeutic target in future to inhibit pancreatitis. |
