Abstract
The intronic microRNA (miR)-342 has been proposed as a potent tumor-suppressor gene. miR-342 is found to be downregulated or epigenetically silenced in multiple different tumor sites, and this loss of expression permits the upregulation of several key oncogenic pathways. In several different cell lines, lower miR-342 expression results in enhanced proliferation and metastasis potential, both in vitro and in xenogenic transplant conditions. Here, we sought to determine the function of miR-342 in an in vivo spontaneous cancer model, using the Ela1-TAg transgenic model of pancreatic acinar carcinoma. Through longitudinal magnetic resonance imaging monitoring of Ela1-TAg transgenic mice, either wild-type or knockout for miR-342, we found no role for miR-342 in the development, growth rate, or pathogenicity of pancreatic acinar carcinoma. These results indicate the importance of assessing miR function in the complex physiology of in vivo model systems and indicate that further functional testing of miR-342 is required before concluding it is a bona fide tumor-suppressor-miR.
Highlights
Cancer development and growth involves the coordinated dysregulation of multiple cellular processes, including proliferation, apoptosis, migration, immune evasion, genome stability, metabolism, and angiogenesis
Pancreatic cancer represents an important therapeutic target, with radically different expression of several miRs [3] and a distinct paucity of effective treatments leading to poor prognosis [4]
Through longitudinal magnetic resonance imaging (MRI) assessment, we found no evidence for a tumorsuppressor role for miR-342 in the Ela1-TAg transgenic model
Summary
Cancer development and growth involves the coordinated dysregulation of multiple cellular processes, including proliferation, apoptosis, migration, immune evasion, genome stability, metabolism, and angiogenesis. Pancreatic cancer represents an important therapeutic target, with radically different expression of several miRs [3] and a distinct paucity of effective treatments leading to poor prognosis [4]. It is a promising line of research to functionally investigate the known miR expression changes in pancreatic cancer. The breadth of cancers observed to show expression changes in miR-342 suggests a common oncogenic function for these changes, mediated by altered regulation of the target mRNA It should, be noted that miR-342 expression is coordinated with the host gene, EVL [17], and even if the observed correlation is functional it may not indicate an oncogenic role specific to miR-342. Through longitudinal magnetic resonance imaging (MRI) assessment, we found no evidence for a tumorsuppressor role for miR-342 in the Ela1-TAg transgenic model
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
