Fig. 8: Inactivation of WDR5 by knockdown or WDR5i inhibits stemness and proliferation of MCF-7 cells and promotes fulvestrant’s anticancer activity. | Cell Death & Differentiation

Fig. 8: Inactivation of WDR5 by knockdown or WDR5i inhibits stemness and proliferation of MCF-7 cells and promotes fulvestrant’s anticancer activity.

From: The PML1-WDR5 axis regulates H3K4me3 marks and promotes stemness of estrogen receptor-positive breast cancer

Fig. 8

Knockdown of WDR5 reduces stem cell populations (A) and the proliferation (B), and fulvestrant’s IC50 (C) in MCF-7 cells. OICR-9429 and C16 treatments reduce stem cell population (D) and stemness-related gene expression (E) of MCF-7 cells. PML1 rescues the proliferation of OICR-9429- (F) and C16-treated cells (G). OICR-9429 and C16 significantly enhance fulvestrant’s anticancer activity of PML1 stably expressing MCF-7 cells (H). IC50 for Ful, Ful plus OICR9429, and Ful plus C16 are 2.511e-008, 1.120e-010, and 1.447e-009, respectively. The IC20 of OICR9429 (2.5 μM) or C16 (1.25 μM) was used in combination with fulvestrant. Most experiments were analyzed using Two-way ANOVA, whereas IC50 data were analyzed using Prism 9 for dose-response curve fitting and calculation of IC50 values. Each experiment was performed with N = 3 in each group.

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