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MiR-124 inhibits cell proliferation, migration and invasion by directly targeting SOX9 in lung adenocarcinoma.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Wang, Xiaoying Liu, Yanli Liu, Xiaoli Yang, Jingyan Teng, Guoxin Zhang, Lulu Zhou, Chengjun |
| Copyright Year | 2016 |
| Abstract | Accumulating evidence indicates that dysregulation of microRNAs (miRNAs) may contribute to the initiation and progression of cancer. However, the role of miR-124 in lung adenocarcinoma (ADC) and the underlying mechanisms through which miR-124 exerts its functions are not completely understood. In the present study, we detected miR-124 and SOX9 expression in lung ADC tissues. The results showed that miR-124 was significantly downregulated in the lung ADC tissues compared with that noted in the corresponding non-cancerous lung tissues and the level of SOX9 protein was inversely associated with the expression of miR-124. The study in human lung ADC cell line A549 demonstrated that upregulation of miR-124 could inhibit cell proliferation, migration and invasion. The bioinformatic analysis showed that there was a putative miR-124 binding site in the 3' untranslated region (3'UTR) of SOX9. Using a luciferase reporter assay, we verified that SOX9 is a direct target of miR-124. Furthermore, overexpression of miR-124 repressed SOX9 expression, whereas inhibition of miR-124 increased expression of SOX9 in the A549 cells. Finally, we identified that SOX9 was a functional mediator of miR-124 in A549 cells. Taken together, our results suggest that miR-124 functions as a tumor suppressor in lung ADC by directly targeting SOX9 and it may be a promising candidate for miR‑based therapy against lung ADC. |
| File Format | PDF HTM / HTML |
| DOI | 10.3892/or.2016.4648 |
| PubMed reference number | 26935152 |
| Journal | Medline |
| Volume Number | 35 |
| Issue Number | 5 |
| Alternate Webpage(s) | https://www.spandidos-publications.com/or/35/5/3115/download |
| Journal | Oncology reports |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
