Conclusions
Our data suggested that Tanshinone IIA induced cell apoptosis in ovarian carcinoma TOV-21G cells via direct upregulation of miR-205. Our study highlighted the potential therapeutic application of Tanshinone IIA against ovarian malignancy.
Methods
The cell survival upon Tanshinone IIA treatment was determined by the clonogenic assay. Cell apoptosis was analysed by Annexin V/propidium iodide double staining. The cleaved caspase-3/poly ADP-ribose polymerase and apoptosis-related factors were quantified by Western blotting. The relative expression of microRNAs (miRs) was determined by real-time polymerase chain reaction. Key findings: Tanshinone IIA treatment induced significant apoptosis in TOV-21G cells. Tanshinone suppressed survivin expression while not affected Bax, Bcl-2 and Bcl-xL. We further predicted and experimentally confirmed overexpression of miR-205 in TOV-21G, which ectopic significantly inhibited survivin and promoted cell apoptosis. miR-205-specific antagonist completely abrogated the cell suppressive effect of Tanshinone IIA. Conclusions: Our data suggested that Tanshinone IIA induced cell apoptosis in ovarian carcinoma TOV-21G cells via direct upregulation of miR-205. Our study highlighted the potential therapeutic application of Tanshinone IIA against ovarian malignancy.