Fig. 3

Evaluating FKA as a candidate drug for targeting PRMT5. a PRMT5 candidate inhibitors ranked by docking score. b Docking model exhibited the binding model between FKB and PRMT5. c Chemical structure of FKA. d Cell viability assay performed after treatment with FKA, and FKA IC50 were calculated in T24 (left) and UMUC3 (right). Data are presented as the mean ± SD of three replicates. e PRMT5 expression changes after treatment with different concentrations of FKA at different times, in T24 (left) and UMUC3 (right). f Cell viability measured in T24 (upper) and UMUC3 (lower) after PRMT5 expression knockdown or treatment with 40 μM FKA. FKA treatment rescue effect tested in BC cells overexpressing PRMT5. Data are presented as the mean ± SD of three replicates. ** p < 0.01, *** p < 0.001, using one-way ANOVA test. g Cell apoptosis measured after PRMT5 expression knockdown, 40 μM FKA treatment, and FKA treatment in T24 overexpressing PRMT5 using flow cytometry (left). Apoptosis rates for replicated assays were counted (right). Data are presented as the mean ± SD of three replicates. ** p < 0.01, *** p < 0.001, using Student’s t-test. h Cell viability changes after treatment with 40 μM FKA, two PRMT5 inhibitors and BC first-class chemotherapy drug. Synergetic effect on cell viability upon co-treatment with FKA or PRMT5 inhibitors and GC in T24 (left) and UMUC3 (right). Data are presented as the mean ± SD of three replicates. ** p < 0.01, *** p < 0.001, using one-way ANOVA test. i BC regulon gene changes after adding FKA to T24, measured using PCR, and the fold changes were standardized and normalized by log10. Data are presented as the mean ± SD of three replicates