Abstract
BACKGROUND: This study aimed to investigate the clinical characteristics of miR-450b-3p in the patients of gastric cancer (GC), and further explore whether miR-450b-3p could inhibit the proliferation of GC cells via regulating KLF7. METHODS: Real-time quantitative PCR (qRT-PCR) was performed to detect the expression level of miR-450b-3p in 48 GC patients of tumor tissue and paracancerous tissue specimens collected, and the associations between miR-450b-3p and the clinical characteristics of GC patients were analyzed. Meanwhile, the expression of miR-450b-3p in GC cell lines was verified using qRT-PCR. miR-450b-3p overexpression vectors was constructed in GC cell lines including AGS and BGC-823, and then CCK-8 cell proliferation assay, Plate colony formation assay and EdU assay were applied to analyze the biological function of miR-450b-3p in GC cell lines. RESULTS: The results of qRT-PCR showed that the expression level of miR-450b-3p in GC tissues was lower than that in paracancerous tissues, and the difference was statistically significant. Compared with GC patients with high-miR-450b-3p expression, these GC patients with low-miR-450b-3p expression had a higher pathological stage and tumor size. Subsequently, the proliferation ability of GC cells in miR-450b-3p mimic was significantly decreased when comparing with the NC mimic. In addition, qRT-PCR indicated that the expression level of KLF7 significantly decreased after miR-450b-3p mimic. Therefore, it was demonstrated that miR-450b-3p might inhibit the malignant progression of GC via modulating KLF7. Bioinformatics analysis and dual luciferase reporter suggested miR-450b-3p was bound to KLF7. Finally, the results of the reverse experiment confirmed that overexpression of KLF7 could reverse miR-450b-3p mimic induced-inhibition of GC malignant progression. CONCLUSIONS: Generally, miR-450b-3p significantly down-regulated in GC tissues and cell lines, and was associated with the pathological stage and tumor size of GC patients. Meanwhile, miR-450b-3p inhibited cell proliferation in GC via modulating KLF7.