Galectin-1-driven upregulation of SDF-1 in pancreatic stellate cells promotes pancreatic cancer metastasis. (1st July 2017)

• Record Type: Journal Article
• Authors: Qian, Dong; Lu, Zipeng; Xu, Qingcheng; Wu, Pengfei; Tian, Lei; Zhao, Liangtao; Cai, Baobao; Yin, Jie; Wu, Yang; Staveley-O'Carroll, Kevin F.; Jiang, Kuirong; Miao, Yi; Li, Guangfu
• Is Part Of: Cancer letters. Volume 397(2017)
• Page Start: 43
• Page End: 51
• Publication Date: 2017-07-01
• Subjects: Galectin-1 -- SDF-1 -- Pancreatic stellate cell -- Pancreatic cancer -- Metastasis; Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.canlet.2017.03.024
• Languages: English
• ISSNs: 0304-3835

Abstract

Abstract: Galectin-1, mainly expressed in activated pancreatic stellate cells (PSCs), is involved in many important cancer-related processes. However, very little is known how Galectin-1 modulates PSCs and subsequently impacts pancreatic cancer cells (PCCs). Our chemokine antibody array and in vitro studies demonstrates that Galectin-1 induces secretion of stromal cell-derived factor-1(SDF-1) in PSCs by activating NF-κB signaling. The secreted SDF-1 increases migration and invasion of PCCs. Knockdown of Galectin-1 and inhibitor-mediated blockade of SDF-1 as well as its ligand CXCR4 and NF-κB verifies the findings. In vivo experiment by knockdown of Galectin-1 in PSCs further demonstrates the conclusion. Collectively, the present studies demonstrate that Galectin-1-driven production of SDF-1 in PSCs through activation of NF-κB promotes metastasis in PDAC, offering a potential target in the treatment of pancreatic cancer. Highlights: In our study, silencing Galectin-1 suppressed PSC-augmented invasion and inhibited tumor progression. By chemokine array, we demonstrated that treatment with Galectin-1 increased the secretion of SDF-1. Our exploration of the potential mechanism indicated that this effect was induced via activation of NF-κB.