miR-145 suppresses colorectal cancer cell migration and invasion by targeting an ETS-related gene
MicroRNA-145 (miR-145) has been demonstrated to be downregulated in various cancer types including colorectal cancer (CRC). However, the function of miR-145 in CRC has not been clearly elucidated. In this study, we examined miR-145 expression by quantitative real-time PCR (qRT-PCR) in CRC cell lines...
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Veröffentlicht in: | Oncology reports 2016-10, Vol.36 (4), p.1917-1926 |
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Sprache: | eng |
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Zusammenfassung: | MicroRNA-145 (miR-145) has been demonstrated to be downregulated in various cancer types including colorectal cancer (CRC). However, the function of miR-145 in CRC has not been clearly elucidated. In this study, we examined miR-145 expression by quantitative real-time PCR (qRT-PCR) in CRC cell lines as well as tumors and corresponding normal mucosa, and the results were correlated to the clinicopathological parameters. In addition, using computational algorithms we investigated putative miR-145 targets. The role of miR-145 was further examined in studies in vitro. In our study miR-145 was significantly decreased in CRC tissues and cell lines compared with non-cancerous colorectal mucosa, especially lymph node or distance metastasis cases. Based on computational algorithms, we assumed that ERG was directly modulated by miR-145 in colorectal cancer cells. For the first time, we demonstrated that ERG was highly expressed in CRC tissues compared with normal ones by qRT-PCR. The inverse correlation between the expression of miR-145 and ERG was observed in CRC tissues. Dual-Luciferase assays demonstrated the direct interaction between miR-145 and 3′-UTR of ERG mRNA. Ectopic expression of miR-145 suppressed the proliferation and invasion ability of colorectal cancer cells, while ERG knockdown partially restored the tumor suppressive effect of miR-145. These results suggested that miR-145 might act as a tumor suppressor during the process of CRC malignant transformation by interacting with ERG. |
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ISSN: | 1021-335X 1791-2431 |
DOI: | 10.3892/or.2016.5042 |