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. 2021 Jul 14;12(7):704. doi: 10.1038/s41419-021-03978-0

Fig. 2. STL inhibits FOXM1 expression on protein level via autophagy-dependent mechanism.

Fig. 2

a C3-luc cells stimulated with doxycycline to induce expression of EGFP-FOXM1 fusion protein were treated with increasing concentrations of STL for 24 h. Total protein samples were analyzed via immunoblotting for FOXM1 and GFP expression, β-actin was used as an internal loading control. b Doxycycline-stimulated C3-luc cells were treated with 50 μM STL for 6 or 24 h and 10 μg/mL ActD for 6 h. Total RNA samples were analyzed for FOXM1, GFP, and MCL1 transcript levels via RT-qPCR, 18 S rRNA was used as a reference transcript. Data are presented as means ± S.D. and individual datapoints, N = 4, * – exact p = 0.02857 (Mann–Whitney U test, two-tailed). c C3-luc cells were treated with indicated concentrations of doxycycline, STL, or CHX for 24 h. Total protein samples were analyzed via immunoblotting for FOXM1, NPM, and MCL1 expression, β-actin was used as an internal loading control. d Doxycycline-stimulated C3-luc cells were treated with STL for 24 h in the presence of bortezomib or MG132. Total protein samples were analyzed via immunoblotting for FOXM1 expression, β-actin was used as an internal loading control. e Doxycycline-stimulated C3-luc cells were treated with STL for 24 h in the presence of bafilomycin A1. Total protein samples were analyzed via immunoblotting for FOXM1 expression, β-actin was used as an internal loading control.