Tandon, M. et al. (2019) Prolactin promotes fibrosis and pancreatic cancer progression. Cancer Research, 79(20), pp. 5316-5327. (doi: 10.1158/0008-5472.CAN-18-3064) (PMID:31395607) (PMCID:PMC6801092)
Full text not currently available from Enlighten.
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is associated with significant fibrosis. Recent findings have highlighted the pro-fibrotic activity of tissue-resident macrophages in the pancreatic cancer microenvironment. Here, we showed that neoplastic pancreatic epithelium, as well as a subset of tissue-resident macrophages, express the prolactin receptor (PRLR). HMGB1-induced prolactin expression in the pancreas maintained FAK1 and STAT3 phosphorylation within the epithelium and stroma. Gain-of-function and loss-of-function experiments demonstrated the essential role of prolactin in promoting collagen deposition, and fibrosis. Finally, the signaling cascade downstream of Prolactin/PRLR activated STAT3 rather than STAT5 in PDAC. These findings suggest that targeting prolactin together with IL-6, a known major activator of STAT3, could represent a novel therapeutic strategy for treating pancreatic cancer.
| Item Type: | Articles |
|---|---|
| Status: | Published |
| Refereed: | Yes |
| Glasgow Author(s) Enlighten ID: | Bailey, Dr Peter and Biankin, Professor Andrew |
| Authors: | Tandon, M., Coudriet, G. M., Criscimanna, A., Socorro, M., Eliliwi, M., Singhi, A. D., Cruz-Monserrate, Z., Bailey, P., Lotze, M. T., Zeh, H., Hu, J., Goffin, V., Gittes, G. K., Biankin, A. V., and Esni, F. |
| College/School: | College of Medical Veterinary and Life Sciences > School of Cancer Sciences |
| Journal Name: | Cancer Research |
| Publisher: | American Association for Cancer Research |
| ISSN: | 0008-5472 |
| ISSN (Online): | 1538-7445 |
| Published Online: | 08 August 2019 |
University Staff: Request a correction | Enlighten Editors: Update this record
Funder and Project Information
Funder and Project Information