Conclusion
MALAT1 promotes EOC cells' survival by downregulating miR-145-5p so it may become a new direction for EOC diagnosis and gene therapy.
Methods
MALAT1 and miR-145-5p expression in the tissues, serum, and EOC cell lines (TOV-112D, TOV-21G) of patients with EOC were detected. The two genes were transfected into the cells via upregulating or downregulating their expression. Levels of apoptosis-related proteins (Caspase-3, Bax, Bcl-2) were analyzed. Mechanisms of cell proliferation, invasion, and apoptosis were studied.
Purpose
This paper was aimed at investigating the regulatory mechanism of long non-coding RNA metastasis-associated lung adenocarcinoma transcript-1 (MALAT1) in epithelial ovarian cancer (EOC). Materials and
Results
MALAT1 was high expressed in EOC tissues, while miR-145-5p was poorly expressed in them. The areas under the curves (AUCs) of the two genes for diagnosing EOC were greater than 0.850, and the two had a significantly negative correlation. According to multivariate Cox regression analysis, high MALAT1 expression, tumor size, degree of differentiation, case staging, and lymph node metastasis were the independent risk factors affecting prognosis. The 5-year overall survival rate (OSR) of patients with low MALAT1 expression was remarkably higher than that of those with high expression. Overexpressing miR-145-5p and silencing MALAT1 could inhibit EOC cells from proliferating and invading, increase their apoptotic rate, and improve levels of the apoptosis-related proteins. After co-transfection with MALAT1-inhibitor + miR-145-5p-inhibitor, the proliferation and invasion of TOV-112D and TOV-21G cells were inhibited and the apoptotic rate rose more obviously. Inhibiting MALAT1 could increase miR-145-5p expression, thus inhibiting EOC cells from proliferating and invading and thereby increasing their apoptotic rate.