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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: Biochem Pharmacol. 2018 Dec 19;160:134–145. doi: 10.1016/j.bcp.2018.12.014

Fig. 2. Inhibition of m6A methylation increased Dox-induced apoptosis in TP53-Dox cancer cells.

Fig. 2.

SW48-Dox and TP53-Dox cells were treated with neplanocin A (NPC, 20 nM) or vehicle for 3 days, and then exposed to Dox (100 nM, for 48 h) with these treatments to induce apoptosis. Imaging flow cytometry was accomplished with an ImageStream X Mark II system, and the data analyzed with IDEAS® Software. A, Apoptosis assay with imaging flow cytometry. BrdU, bromodeoxyuridine-FITC; BF, bright field; PI, propidium iodide. Top-panel, images of apoptotic and nonapoptotic cells of TP53-Dox cells identified using imaging flow cytometry for analysis. Apoptotic cells labelled with BrdU-FITC (green) are presented as percentages of total cells detected in each sample. B, NPC effects on apoptosis. **, p<0.001 compared to SW48-Dox cells; *, p<0.001 compared to cells treated with vehicle. C, Representative Western blot of PARP protein. After above treatments, equal amounts of detergent-soluble proteins extracted (50 μg/lane) were resolved using 4–20% gradient SDS-PAGE, and then immunoblotted with PARP antibody. Cleaved-P, cleaved PARP; GAPDH served as internal control. Protein levels (bottom panel) are represented as means of their optical densities normalized against GAPDH from three settings of blots. *, p<0.01 compared to corresponding cells treated with vehicle.