Fig 1: Secondary validation. (A) Effects of compound 4 (3.2 µm) on mark H3K79me2 and H3R2me2a in U2OS cells evaluated by western blotting assay following eight days of treatment. The error bars indicate the standard deviation between two biological replicates. (B) Effects of compound 4 on mark H3K79me2 in U2OS cells at 1 µm, 3.2 µm, respectively, measured by FACS after ten days of treatment. (C), (D) Co-immunoprecipitation of endogenous DOT1L (C) and CARM1 (D) in U2OS cells treated by compound 4 (3.2 µm) and EPZ-5676 (3.2 µm) after eight days treatment. The graph represents the intensity of the selected HMTs of the treated cells normalised to DMSO. The error bars indicate the standard deviation between two biological replicates. (E), (F) Co-immunoprecipitation of histone mark H3K79me2 (E) and H3R2me2a (F) in U2OS cells treated with compound 4 (3.2 µm) after eight days treatment. Cells treated with an equal amount of DMSO were used as negative control. The graph represents the intensity of the mark or histone H3 of the treated cells normalised to DMSO. The error bars indicate the standard deviation between two biological replicates.
Fig 2: Up-regulation of lncRNA RP11-545G3.1 in nasopharyngeal carcinoma and the effects of its knockdown on nasopharyngeal carcinoma cell viability. (A) RT-qPCR analysis of the expression of RP11-545G3.1 in 21 paired nasopharyngeal carcinoma and normal specimens. (B) RT-qPCR analysis of the expression of RP11-545G3.1 in nasopharyngeal carcinoma cells and normal cells. (C) Assessment of the silencing effects of shRNAs against RP11-545G3.1 in CNE-2 and NP69 cells by RT-qPCR. (D, E) CCK-8 assay of the cell viability of CNE-2 and NP69 cells transfected with shRNAs against RP11-545G3.1. (F−H) Western blot showing the expression of CARM1, CCND2 and P21 in CNE-2 and NP69 cells transfected with shRNAs against RP11-545G3.1. **P < 0.01; ***P < 0.001; ****P < 0.0001
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