Skip to main content
. 2022 Mar 10;30(7):2603–2617. doi: 10.1016/j.ymthe.2022.03.003

Figure 1.

Figure 1

PRMT5 inhibits doxorubicin-induced RNA m6A methylation

(A) Left: dot-blot assay of RNA m6A methylation in breast cancer patient samples with (n = 15) or without (n = 18) neoadjuvant doxorubicin (DOX) therapy. Right: semiquantification of the data shown at the left. (B) Semiquantification of the data from a dot-blot assay of RNA m6A methylation in breast cancer tissue samples from a PDX mouse model treated with or without DOX. (C) Dot-blot assay of RNA m6A methylation in MDA-MB-231 and T47-D breast cancer cells treated with DOX for the duration and dose indicated. (D) Dot-blot assay of RNA m6A methylation in MDA-MB-231, MCF-7, and T47-D breast cancer cells overexpressing PRMT5 treated with doxorubicin as indicated. MDA-MB-231, 0.4 μg/mL DOX for 24 h; MCF-7 and T47-D, 0.5 μg/mL DOX for 24 h. (E) Dot-blot assay of RNA m6A methylation in wild-type and prmt5-knockout MEFs treated with 0.4 μg/mL DOX for 24 h. An anti-m6A antibody was used for dot blots with 200 ng of mRNA, and methylene blue staining was used as the loading control in (A), (C), (D) and (E).