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. Author manuscript; available in PMC: 2019 Aug 10.
Published in final edited form as: Cancer Lett. 2018 May 5;429:1–10. doi: 10.1016/j.canlet.2018.04.041

Figure 6. The ASPH specific inhibitor, MO-I-1151 suppressed RB1 phosphorylation without affecting histone methylation in contrast to other inhibitors of 2-OG-dependent dioxygenases.

Figure 6

The pRB1s780, RB1, and α-tubulin proteins were determined in serum starved H1 cells which were harvested 4 hours post challenges with (A) 0.5mM, 1mM DMOG, 50µM, 100µM DFO, (B) 5µM, or 10µM MO-I-1151. (C) pRB1s780, RB1, IDH1, flag-tag, and GAPDH were measured in HEK-293T cells transfected with EV, flag-IDH1, flag-IDH1 mutated (IDH1mut). (D) ASPH, H3K9Me2, H3K4Me3, and H3 were determined in H1 cells transduced with shLuc or shASPH. The expression levels of H3K9Me2, H3K4Me3, and H3 were evaluated in H1 cells treated with (E) 5, 10 µM MO-I-1151, (F) 0.5, 1mM DMOG, 50, or 100µM DFO for 24 hours. (G) The results of H3K9Me2, H3K4Me3, flag-IDH1, and GAPDH in HEK-293T cells transfected with EV, IDH1, or IDH1mut for 24 hours were shown. (H) A cartoon illustrates the actions of targeting ASPH by different strategies in the protein interaction between RB1 and CDK complexes (RB1com) as well as RB1 phosphorylation.