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.
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.
Entities:
Keywords:
Esophageal squamous cell carcinoma; Invasion; Metastasis; MiR-1290; MicroRNA; Suppressor of cancer cell invasion
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