AI Article Synopsis
- Chronic inflammation is linked to pancreatic cancer, and recent research shows that the immune signaling pathway involving IL22/IL22RA1 plays a crucial role in the disease's progression and patient outcomes.
- High expression of IL22RA1 in pancreatic cancer cells correlates with a worse prognosis and increased cancer stemness, indicating a more aggressive tumor behavior.
- The IL22RA1/STAT3 signaling pathway is essential for maintaining the cancer stem cells, suggesting potential therapeutic targets for patients with high levels of IL22RA1 in pancreatic ductal adenocarcinoma (PDAC).
Article Abstract
Chronic inflammation is a feature of pancreatic cancer, but little is known about how immune cells or immune cell-related signals affect pancreatic cancer stemness and development. Our previous work showed that IL22/IL22RA1 plays a vital role in acute and chronic pancreatitis progression by mediating cross-talk between immune cells and acinar cells or stellate cells, respectively. Here, we find IL22RA1 is highly but heterogeneously expressed in pancreatic cancer cells, with high expression associated with poor prognosis of patients with pancreatic cancer. The IL22RA1 population from pancreatic cancer harbored higher stemness potential and tumorigenicity. Notably, IL22 promoted pancreatic cancer stemness via IL22RA1/STAT3 signaling, establishing the mechanism of regulation of cancer stemness by microenvironmental factors. Moreover, STAT3 was indispensable for the maintenance of IL22RA1 cells. Overall, these findings provide a therapeutic strategy for patients with PDAC with high expression of IL22RA1. IL22RA1/STAT3 signaling enhances stemness and tumorigenicity in pancreatic cancer. .
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1158/0008-5472.CAN-17-3131 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!