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. 2019 Sep 30;55(6):1296–1312. doi: 10.3892/ijo.2019.4887

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Copyright: © Ye et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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miR-421 enhances the inhibitory effect of anisomycin on HuOCSCs. (A) MTT results showed that overexpression of miR-421 and treatment with anisomycin resulted in more severe proliferation inhibition of HuOCSCs, than either treatment alone. ^**P<0.01 vs. DMSO group (n=4). (B) Quantitative PCR results showed that overexpression of miR-421 and treatment with anisomycin decreased the expression of lncRNA-Meg3, PDGFRA, Notch1, HES1 and RBPJ. ^**P<0.01 vs. DMSO group (n=4). (C) Schematic of the proposed molecular mechanism of anisomycin inhibition of the activity and angiogenesis of ovarian cancer cells, by attenuating the molecular sponge effect in the lncRNA-Meg3/miR-421/PDGFRA axis. miR, microRNA; HuOCSCs, human ovarian cancer stem cells; lncRNA, long non-coding RNA; Meg3, maternally expressed 3; PDGFRA, platelet derived growth factor receptor α; HES1, hes family bHLH transcription factor 1; RBPJ, recombination signal binding protein for immunoglobulin κ J region; mut, mutant.