Published online Mar 21, 2015. doi: 10.3748/wjg.v21.i11.3245
Peer-review started: August 9, 2014
First decision: September 27, 2014
Revised: October 11, 2014
Accepted: December 16, 2014
Article in press: December 16, 2014
Published online: March 21, 2015
AIM: To investigate the biological role of miR-1290 in esophageal squamous cell carcinoma (ESCC) progression and invasion and the underlying mechanism.
METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate miR-1290 expression in ESCC tissue samples. The roles of miR-1290 in cell proliferation, migration and invasion were identified using miR-1290 mimic-transfected cells. In addition, the regulatory effect of miR-1290 on suppressor of cancer cell invasion (SCAI) was evaluated using qRT-PCR, Western blot analysis and a dual luciferase reporter assay.
RESULTS: miR-1290 was significantly upregulated in ESCC tissue samples compared with normal adjacent tissues (9.213 ± 1.150 vs 1.000 ± 0.0), (P < 0.01). Upregulation of miR-1290 was associated with tumor differentiation (P = 0.021), N classification (P = 0.006) and tumor-node-metastasis stage (P = 0.021) in ESCC patients. Moreover, ectopic miR-1290 expression potently promoted ESCC cell growth (P < 0.01), migration (P < 0.01) and invasion (P < 0.01) in vitro. miR-1290 overexpression in ESCC cell lines decreased SCAI expression at the translational level and reduced SCAI-driven luciferase-reporter activity (P < 0.01).
CONCLUSION: Our findings suggested that miR-1290 may play an oncogenic role in cellular processes of ESCC.
Core tip: In this study, we reported the clinical significance and biological effects of miR-1290 in esophageal squamous cell carcinoma (ESCC). We found that miR-1290 was significantly up-regulated in ESCC tissues. Moreover, we showed that ectopic expression of miR-1290 significantly promoted ESCC cell growth, migration and invasion. Further investigation revealed that suppressor of cancer cell invasion was a downstream target of miR-1290.