Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and deadly neoplasias. The aggressiveness of PDAC is in part due to the interaction between cancer cells and pancreatic stellate cells (PSCs). PSCs are responsible for the so called desmoplasia, which is an excessive deposition of extracellular matrix within the tumor. Desmoplasia facilitates metastasis and prevents effective chemotherapeutic drug delivery. Our aim was to determine how the activity of PSCs is altered by growth factors frequently found in PDAC.

We isolated primary murine PSCs and confirmed their identity by revealing the expression of alpha smooth muscle actin and the presence of vitamin a droplets.

Stellate cells become activated by stimulants that are released by pancreatic cancer cells. To reveal stimulation we measured the change in the cells’ motility in response to PDGF and EGF using time lapse video microscopy. Additionally, we investigated whether PSCs were able to chemotax towards those stimulants.

Our findings show that both PDGF and EGF are potent stimulants of PSC migration. Although both growth factors increase translocation (net distance covered during the experiment), only EGF was able to increase the speed of movement. These results were confirmed in chemotaxis experiments. Here, too, translocation and speed were increased by PDGF and EGF. Both growth factors induce chemotaxis, with PDGF being the more potent chemokine.

These results show that PDGF and EGF stimulate murine PSCs and that PDGF is a potent chemokine for PSCs. Thus inhibition of these pathways might affect PDAC by decreasing PSCs’ activity.