MicroRNAs (miRNAs) participate in post-transcriptional regulation by targeting the 3′ untranslated region of target genes that are involved in diverse biological processes. To the best of our knowledge, the association between miR-152 and ERBB3 in ovarian cancer remains unclear. In the present study, a negative correlation between miR-152 and ERBB3 in ovarian cancer was observed. The luciferase reporter gene assay results demonstrated that miR-152 negatively regulated ERBB3 in SKOV3 and OVCAR3 ovarian cancer cells. Furthermore, our results revealed that miR-152 suppressed the ability of ovarian cancer cell proliferation, migration and invasion, and promoted apoptosis through inhibiting ERBB3 in vitro. Therefore, in the present study, miR-152 was found to be involved in the proliferation and metastasis of ovarian cancer cells through repression of ERBB3 expression. Therefore, miR-152 may be a potential therapeutic target for the treatment of ovarian cancer.
Ellagic acid has been reported to possess various activities, including anti-inflammatory, anti-oxidative, antiviral and anticancer abilities. However, the effect and underlying molecular mechanism of ellagic acid on cervical carcinoma remain unclear. Therefore, the present study aimed to investigate the effects of ellagic acid on human cervical carcinoma cells and the molecular mechanism involved. The present study assessed the survival of HeLa cells cultured in vitro using an MTT assay. Apoptosis rate and cell cycle of HaLa cells were measured using an Annexin V-Fluorescein isothiocyanate/propidium iodide Apoptosis Detection and Cell Cycle Analysis kits, respectively, following treatment with varying concentrations of ellagic acid. Further effects of ellagic acid on HeLa cells was assessed using flow cytometry and western blotting. Ellagic acid treatment significantly inhibited cell proliferation of the human cervical carcinoma HeLa, SiHa and C33A cells. In HeLa cells, it was observed that ellagic acid arrested the cell cycle at G1 phase, induced cell apoptosis, suppressed the phosphorylation of Janus kinase 2 and signal transducer and activator of transcription 3 (STAT3), as well as modulated the expression of associated proteins. Collectively, the results of the present study provide evidence that ellagic acid inhibits cervical carcinoma cell proliferation, and induces apoptosis and cell cycle arrest at G1 phase possibly via the regulation of STAT3 signaling.
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