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. 2018 Dec 5;9:5200. doi: 10.1038/s41467-018-07258-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — AKTi induces CDK6 expression. a A proposed model illustrating the interplay of FOXO3a-AKT-SirT6, which leads to the formation of the FOXO3a-BRD4 complex (left panel). WT, S338A, or S338E mutant of SirT6 were expressed in indicated cells followed by treatment with 1 μM MK2206 for 4 days. The growth suppressive effects were examined by cell count analyses. SirT6 expression was confirmed by western blotting. Data presented are representative of three experiments performed in triplicate as the mean ± SD. ^*p < 0.01 (MK2206-treated group is compared with control group without treatment); ^#p > 0.05 (MK2206-treated S338A-SirT6 group is compared with control group without treatment); and ^**p < 0.01 (MK2206-treated S338E-SirT6 group is compared with MK2206-treated vector and WT-SirT6 groups). b BT474 and T47D cells were treated with 1 μM MK2206 for 3 days, differentially expressed genes with more than 2.5-fold changes on RNA-sequencing analysis (GSE118148) from both cell lines were used to identify potential FOXO3a target genes shown in the heat-map. c BT474, T47D, and ZR75 cells were treated with 1 μM MK2206 for 3 days. The mRNA and protein levels of CDK6 were analyzed by RT-PCR and western blotting, respectively. Data presented are representative of three experiments performed in triplicate as the mean ± SD. ^*p < 0.01 when MK2206-treated group is compared with control group. d BT474 cells were treated with 1 μM MK2206 for different time intervals. CDK6 expression was analyzed by western blotting. e E2F driven luciferase reporter was expressed in indicated cells treated with MK2206, JQ1, Palbociclib (PD), or in combination. Luciferase activities were determined by dual luciferase assay. Data presented are representative of three experiments performed in triplicate as the mean ± SD. ^*p < 0.01 when MK2206-treated group is compared with other groups. f BT474 and T47D cells were treated with MK2206 (1 μM) in the absence or presence of JQ1 or MS417 (1 μM). CDK6 expression was analyzed by western blotting. g BT474 cells were treated with three different AKTi (1 μM) in the absence or presence of JQ1 or MS417 (1 μM). CDK6 expression was analyzed by western blotting