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. 2021 Oct 22;11:20871. doi: 10.1038/s41598-021-00150-8

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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CDK1 contributes to HSP90-mediated HIF1α stabilization. (A) Inhibition of CDK1 decreases the level of HIF1α in RCC4 cells independently of VHL. Cells were treated with Ro-3306 (5 μM) or MG132 (1 μM) or both as indicated for 6 h under normoxia. (B) CDK1 inhibition (for 6 h under hypoxia; 0.5% O₂) impairs the interaction between HIF1α and HSP90. HCT116 cells were treated with MG132 and cultured in hypoxia for 6 h with or without Ro-3306. Cells were fixed and lysed for co-immunoprecipitation analysis. Experiment 2 is a repeated experiment performed under the same conditions as in Experiment 1, with an added control (without HA-HIF1α overexpression). (C) CDK1 inhibition partially reversed heat shock-induced HIF1α expression. HCT116 cells were treated at 40 °C with the indicated inhibitors for 6 h. Geldanamycin was used at 2 μM. Intensity was measured compared to β-Actin in each lane. G: geldanamycin; R: Ro-3306. Statistical analysis was performed using one-way ANOVA supplemented with Tukey test. Mean ± SD was shown. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.