| Objective:Ovarian cancer is the third common malignant tumor ofGynecological oncology,due to lack of specific symptoms,the earlydiagnosis is difficult,while the mortality of advanced ovarian cancer is high.So looking for causes and risk factors and exploring tumor markers to earlydiagnose and predict the prognosis of ovarian cancer have always beenresearch hot spot.This article will investigate the expression level ofmiR-124in ovarian cancer (OC) tissues and its effects on the biologicalfunctions of OC cells.Methods:35paired ovarian cancer tissues and adjacent normal tissueswere collected from the Cancer Hospital of Chongqing Municipality,and allthe collected tissues had complete medical records in tissue bank;Using theQuantitative Realtime-PCR, the expression of miR-124was explored in35paired ovarian cancer tissues and adjacent normal tissues; To restore theexpression of miR-124in OC cell line SKOV3, we transfected cells withmiR-124mimic; The proliferation and apoptosis effects of miR-124onSKOV3cells were evaluated by cell counting kit-8(CCK-8) assays and flowcytometery, respectively; Moreover, the migration and invasion assays wereperformed by Transwell chamber assays.Result:The expression of miR-124was generally decreased in35ovarian cancer tissues (1.5254±1.7054) compared with the adjacent normaltissues (2.9420±3.4422), which had statistical significance (P＜0.05).Overexpression of miR-124through exogenous transfection with miR-124mimic significantly suppressed cell proliferation (P＜0.01), induced cell apoptosis (P＜0.05), and inhibited cell migration and invasion (P＜0.01).Moreover, ectopic miR-124expression significantly suppressed theexpression of PIK3CA and its downstream p-AKT (P＜0.01), while did notinfluence the expression of total AKT（P＞0.05）, which suggest thatoverexpression of miR-124significantly suppressed the PI3K/AKTsignaling pathway in OC cells.Conclusion:The expression of miR-124is significantly decreased inOC tissues, and restored its expression could suppress cell proliferation,migration and invasion, and induced cell apoptosis through, at least partially,suppression of PI3K/AKT signaling pathway. |
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