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. 2021 Dec 13;11:749144. doi: 10.3389/fonc.2021.749144

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Copyright © 2021 Zhao, Li, Qiu, Chen, Wu, Wang, Ma, Song and Kong

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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FOXM1 mediated DDX23-driven malignant progression of ovarian cancer cells. Control siRNAs or DDX23 siRNAs were co-transfected into ovarian cancer cells with PCMV-NC or PCMV-FOXM1 plasmids. (A) Western blotting analysis of DDX23 and FOXM1 expression in four rescue groups of HEY cells. (B, C) overexpression of FOXM1 partially restored the reduced cell proliferation (B) and migration (C) induced by DDX23 silencing. (D) Schematic diagram showing that DDX23 is transcriptionally activated by E2F1. DDX23 promotes ovarian cancer progression by regulating FOXM1C production. Data are presented as mean ± SEM. ns, no significant, ***P < 0.001, ****P < 0.0001.