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. 2017 Jun 15;8(35):57938–57947. doi: 10.18632/oncotarget.18488

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Copyright: © 2017 Matsuda et al.

This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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A. FOXO1 and FOXO3 were increased at protein level in both HCT116-p53(+/+) and -p53(-/-) cells by siRNA-mediated MELK knockdown. B. FOXO1 and FOXO3 were also increased at transcriptional level in both HCT116-p53(+/+) and -p53(-/-) cells by siRNA-mediated MELK knockdown. The asterisk indicates p < 0.01 compared with the corresponding value of the siControl group. C. Using HCT116-p53(-/-) cells, chromatin immunoprecipitation (ChIP) and qPCR were performed to quantify FOXO1- or FOXO3-bound DNA complex on the promoter region of p21 or GAPDH (negative control). The co-immunoprecipitated DNA of each antibody was normalized with that of normal IgG, and then its ratio of siMELK/siControl was calculated. The asterisk indicates p < 0.05 compared with the corresponding value of the GAPDH. D. NCI-H23 and TE4 harboring loss-of-function TP53 mutations showed the increase of FOXO1 and FOXO3 proteins after MELK knockdown.