Prolactin promotes fibrosis and pancreatic cancer progression

Manuj Tandon, Gina M. Coudriet, Angela Criscimanna, Mairobys Socorro, Mouhanned Eliliwi, Aatur D. Singhi, Zobeida Cruz-Monserrate, Peter Bailey, Michael T. Lotze, Herbert Zeh, Jing Hu, Vincent Goffin, George K. Gittes, Andrew V. Biankin, Farzad Esni

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


Pancreatic ductal adenocarcinoma (PDAC) is associated with significant fibrosis. Recent findings have highlighted the profibrotic activity of tissue-resident macrophages in the pancreatic cancer microenvironment. Here, we show that neoplastic pancreatic epithelium, as well as a subset of tissue-resident macrophages, expresses the prolactin-receptor (PRLR). High mobility group box 1-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 IL6, a known major activator of STAT3, could represent a novel therapeutic strategy for treating pancreatic cancer.

Original languageEnglish (US)
Pages (from-to)5316-5327
Number of pages12
JournalCancer research
Issue number20
StatePublished - Oct 15 2019

ASJC Scopus subject areas

  • Oncology
  • Cancer Research


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