| First Author | Faversani A | Year | 2017 |
| Journal | Oncotarget | Volume | 8 |
| Issue | 5 | Pages | 7231-7247 |
| PubMed ID | 27980227 | Mgi Jnum | J:309020 |
| Mgi Id | MGI:6754509 | Doi | 10.18632/oncotarget.13933 |
| Citation | Faversani A, et al. (2017) miR-494-3p is a novel tumor driver of lung carcinogenesis. Oncotarget 8(5):7231-7247 |
| abstractText | Lung cancer is the leading cause of tumor-related death worldwide and more efforts are needed to elucidate lung carcinogenesis. Here we investigated the expression of 641 miRNAs in lung tumorigenesis in a K-Ras(+/LSLG12Vgeo);RERTn(ert/ert) mouse model and 113 human tumors. The conserved miRNA cluster on chromosome 12qF1 was significantly and progressively upregulated during murine lung carcinogenesis. In particular, miR-494-3p expression was correlated with lung cancer progression in mice and with worse survival in lung cancer patients. Mechanistically, ectopic expression of miR-494-3p in A549 lung cancer cells boosted the tumor-initiating population, enhanced cancer cell motility, and increased the expression of stem cell-related genes. Importantly, miR-494-3p improved the ability of A549 cells to grow and metastasize in vivo, modulating NOTCH1 and PTEN/PI3K/AKT signaling.Overall, these data identify miR-494-3p as a key factor in lung cancer onset and progression and possible therapeutic target. |
