Defining the role of SID1 transmembrane family, member 1 (SIDT1) in KrasG12D-driven pancreatic intraepithelial neoplasia (PanIN) - adenocarcinoma progression
Pancreatic ductal adenocarcinoma (PDAC) affects around 8000 adults annually in the UK. Despite advances in surgery and chemotherapy, the outlook for these patients remains essentially unchanged, with few long-term survivors. New interventions are urgently required.
Over 90% of human pancreatic cancers harbour Kirsten-Ras (Kras) mutation. Kras mutation is commonly identified in early pre-malignant lesions and is a key driver of cancer progression. MicroRNAs play a central role in carcinogenesis and levels of microRNA-21 increase as Kras-driven pre-malignant pancreatic lesions develop into cancer. Our group has recently shown that the SIDT1 channel conveys microRNA-21 between cells, leading to non-cell-autonomous gene silencing. Using a panel of innovative in vitro, in vivo and clinical approaches, we now seek to determine the role of SIDT1 in Kras-driven pancreatic cancer. A better understanding of non-autonomous microRNA actions and their role in cancer progression may yield new therapeutic approaches that could avert devastating cancer.
Mohamed Elhassan is a Spire Murrayfield Research Fellow.
He is also supported by the Melville Trust for the Care and Cure of Cancer Research Fellowship.
This project is supervised by Mr M Duxbury.
- Awarded the Innovation Initiative Grant by the University of Edinburgh