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. Author manuscript; available in PMC: 2023 Dec 2.
Published in final edited form as: Cancer Discov. 2023 Jun 2;13(6):1478–1497. doi: 10.1158/2159-8290.CD-22-0825

Figure 6: MLL inhibition reverses TF-1 transformation induced by mutant IDH expression and TET2 loss.

Figure 6:

(A) Proliferation under cytokine-rich conditions of TF-1 cells expressing empty vector (Empty) or HA-tagged R132H-mutant IDH1 (R132H) treated with the indicated concentrations of the MEN1-MLL1 inhibitor VTP50469 or DMSO-control (0 nM). (B) Proliferation under cytokine-poor conditions of TF-1 cells expressing empty vector (Empty), HA-tagged wild-type IDH1 (IDH1), or HA-tagged R132H-mutant IDH1 (R132H) treated with the indicated concentrations of VTP50469 or DMSO-control (0 nM) starting on day 0 of cytokine withdrawal. (C) Proliferation under cytokine-poor conditions of the TF-1 cells from (B) pre-treated with the indicated concentrations of VTP50469 or DMSO-control (0 nM) for two weeks prior to cytokine withdrawal. (D) Immunoblot analysis of trimethyl-H3K4 (H3K4me3) levels in the R132H-mutant expressing TF-1 cells from (C). (E) Proliferation under cytokine-poor conditions of TF-1 cells expressing a non-targeting shRNA (shNT) or a TET2-targeting shRNA (shTET2-1) pre-treated with the indicated concentrations of VTP50469 or DMSO-control (0 nM) for two weeks prior to cytokine withdrawal. (F) Immunoblot analysis of H3K4me3 levels in the TET2-targeting shRNA-expressing TF-1 cells from (E).