Gut Liver.  2012 Oct;6(4):417-422.

Role of Janus Kinase/Signal Transducers and Activators of Transcription in the Pathogenesis of Pancreatitis and Pancreatic Cancer

• Yu JH
• Kim H

Abstract

In the pathogenesis of pancreatitis, oxidative stress is involved in the activation of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway and cytokine expression. High serum levels of cholecystokinin (CCK) have been reported in patients with acute pancreatitis, and treatment with cerulein, a CCK analogue, induces acute pancreatitis in a rodent model. Recent studies have shown that cerulein-activated nicotinamide adenine dinucleotide phosphate oxidase elicits reactive oxygen species, which trigger the phosphorylation of the JAK1, STAT1, and STAT3 proteins and induce the production of inflammatory cytokines, such as tumor necrosis factor-alpha, interleukin (IL)-1beta, and IL-6, in pancreatic acinar cells. The JAK/STAT pathway also stimulates cell proliferation and malignant transformation and inhibits apoptosis in the pancreas. This review discusses the possible role of the JAK/STAT pathway in the pathogenesis of pancreatitis and pancreatic cancer in response to oxidative stress.

Keyword

JAK/STAT; Pancreatitis; Pancreatic cancer; Oxidative stress

MeSH Terms

Acinar Cells
Apoptosis
Caerulein
Cell Proliferation
Cholecystokinin
Cytokines
Humans
Interleukin-6
Interleukins
NADP
Oxidative Stress
Oxidoreductases
Pancreas
Pancreatic Neoplasms
Pancreatitis
Phosphorylation
Reactive Oxygen Species
Rodentia
STAT3 Transcription Factor
Transducers
Tumor Necrosis Factor-alpha
Caerulein
Cholecystokinin
Cytokines
Interleukin-6
Interleukins
NADP
Oxidoreductases
Reactive Oxygen Species
STAT3 Transcription Factor
Tumor Necrosis Factor-alpha