Pancreatic cancer cells are glutamine dependent for growth and proliferation. The glutamine transporter SLC1A5 is upregulated in pancreatic cancer and is being actively investigated as a pharmacological target. We genetically engineered human pancreatic cancer cells to express SLC1A5 shRNA to downregulate SLC1A5. 1H MRS was used to analyze metabolic differences in SLC1A5 downregulated Pa04C_SLC1A5 pancreatic cancer cells and tumors compared to empty vector cells and tumors. SLC1A5 downregulation resulted in a significantly lower glutamine/glutamate ratio in Pa04C_SLC1A5 cells. In Pa04C_SLC1A5 tumors we observed a significant reduction of several metabolites highlighting the metabolic reprogramming that occurred in tumors with SLC1A5 downregulation.
This abstract and the presentation materials are available to members only; a login is required.