Pancreatic Cancer (PC) is a highly metastatic malignancy. Over 80% of PC patients present with advanced-stage disease, preventing potentially curative surgery. The Neuropeptide Y (NPY) system, best known for its role in controlling energy homeostasis1,2, has also been shown to promote tumorigenesis in a range of cancer types3,4, but its role in PC has yet to be explored.
Here, we show that expression of NPY and its receptor NPY1R are upregulated in mouse PC models and human PC patients via q-RT-PCR, chromogenic RNAscope and immunohistochemistry5. Using the genetically engineered, autochthonous KPR172HC mouse model of highly metastatic PC (Pdx1-Cre; LSL-KrasG12D/+; Trp53R172H/+) we demonstrate that pancreas-specific and whole-body knockout of Npy1r significantly decreases metastasis to the liver5. We also observed an increase in adipose and muscle tissue mass in Npy1r knockout settings, providing an additional benefit on top of reducing metastasis in PC, since PC progression is often associated with tissue wasting6.
Transcriptomic and proteomic assessment via RNA-seq and mass spectrometry proteomics, respectively, identified ~500 differentially expressed transcripts and proteins in pancreatic tumours following Npy1r knockout5. While some of these differentially expressed transcripts/proteins have already been shown to have a role in cancer progression and metastasis, many are underexplored in PC warranting further studies based on our datasets.
Complementing our genetic studies, we identify that treatment with the selective NPY1R antagonist BIBO3304 significantly reduces KPR172HC migratory capacity on fibroblast-derived 2.5D cell-derived matrices, which could, in part, be contributing to the anti-metastatic effect observed upon Npy1r knockout in the KPR172HC mouse model5. Importantly, pharmacological NPY1R inhibition in an intrasplenic model of PC metastasis recapitulated the results of our genetic studies, with BIBO3304 significantly decreasing metastasis in the liver in vivo5. Immunohistochemical analysis revealed a significant reduction in cell proliferation5, suggesting that NPY1R inhibition reduces metastasis by decreasing metastatic growth.
Together, our results reveal that NPY/NPY1R signaling is a novel anti-metastatic target in PC. Targeting this pathway may represent a highly effective anti-metastatic strategy for future assessment in conjunction with standard-of-care approaches to improve outcomes for PC patients.