The Role of Smo in Pancreatic Cancer

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The Ohio State University

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Pancreatic Adenocarcinoma (PDAC) remains an overwhelmingly fatal disease with approximately 95% of patients dying within 5 years of diagnosis. Little clinical development has been seen despite the progress that has been made in understanding the molecular makeup of pancreatic cancer. The disease is so deadly because it metastasizes quickly and there is no effective treatment due to the dense stroma that protects the tumor because of an intense desmoplastic reaction. It has been found that the sonic hedgehog (Hh) pathway is upregulated in 70% of pancreatic adenocarcinomas. The sonic Hh ligand is overexpressed in the pancreatic adenocarcinomas and the gene coding for the ligand’s receptor, Smoothened (Smo), is overexpressed in cancer associated fibroblasts. This suggests that cancer associated fibroblasts actively communicate with PDAC tumor cells and that Hh signaling plays some role in PDAC progression. To study the effect of SMO and the crosstalk between the cancer associated fibroblasts (CAFs) and the tumor, PDAC cells were grown in collected conditioned media (CM) harvested from the fibroblasts. Conditioned Media was collected from both SmoWT or Smonull fibroblasts. It was determined through ki67 assays and BrdU assays that when tumor cells were grown in CM form Smonull cellular proliferation increased. Therefore, It was determined that the fibroblasts do communicate with the PDAC cells and when the Hh pathway was removed from the fibroblasts, PDAC proliferation increased.



Pancreatic Cancer