کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5525337 | 1546672 | 2017 | 9 صفحه PDF | دانلود رایگان |
- 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.
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.
Journal: Cancer Letters - Volume 397, 1 July 2017, Pages 43-51