miR-29a-deficiency does not modify the course of murine pancreatic acinar carcinoma
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James Dooley1,2, Vasiliki Lagou1,2, Josselyn E. Garcia-Perez1,2, Uwe Himmelreich3, Adrian Liston1,2
1VIB Center for Brain and Disease Research, Leuven, Belgium
2KU Leuven-University of Leuven, Department of Microbiology and Immunology, Leuven, Belgium
3KU Leuven-University of Leuven, Department of Imaging and Pathology, Molecular Small Animal Imaging Center (MOSAIC), Leuven, Belgium
Adrian Liston, email: firstname.lastname@example.org
Keywords: pancreatic cancer, microRNA, miR-29, in vivo
Received: August 29, 2016 Accepted: February 20, 2017 Published: March 02, 2017
The development of cancers involves the complex dysregulation of multiple cellular processes. With key functions in simultaneous regulation of multiple pathways, microRNA (miR) are thought to have important roles in the oncogenic formation process. miR-29a is among the most abundantly expressed miR in the pancreas. Together with altered expression in pancreatic cancer cell lines and biopsies, and known oncogenic functions in leukemia, this expression data has identified miR-29a as a key candidate for miR involvement in pancreatic cancer biology. Here we used miR-29a-deficient mice and the TAg model of pancreatic acinar carcinoma to functionally test the role of miR-29a in vivo. We found no impact of miR-29a loss on the development or growth of pancreatic tumours, nor on the survival of tumour-bearing mice. These results suggest that, despite differential expression, miR-29a is oncogenically neutral in the pancreatic acinar carcinoma context. If these results are extended to other models of pancreatic cancer, they would reduce the attractiveness of miR-29a as a potential therapeutic target in pancreatic cancer.
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