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. Author manuscript; available in PMC: 2023 Jan 5.
Published in final edited form as: Cancer Res. 2022 Jul 5;82(13):2361–2377. doi: 10.1158/0008-5472.CAN-22-0742

Fig. 7. H2B-D51 oncohistone mutants promote tumor growth in vivo.

Fig. 7.

A) Growth of xenograft tumors formed from MDA-MB-231 cells engineered for ectopic expression of FLAG-tagged WT or D51A mutant H2B in NOD scid gamma (NSG) mice, treated with vehicle or 25 mg/kg Niraparib intraperitoneally (i.p.) 5 days a week over 4 weeks. Each point represents the mean ± SEM (n = 5). Asterisks indicate significant differences at day 28 as indicated (Student’s t-test; ** p < 0.01, *** p < 0.001).

B) Comparison of xenograft tumor volumes at day 28 among different groups as indicated. Each cluster in the plot represents the mean ± SEM (n = 5). Asterisks indicate significant differences as indicated (Student’s t-test; ** p < 0.01, *** p < 0.001, and n.s. not significant).

C) Schematic representation of the mechanism by which PARP-1-mediated ADPRylation of H2B-D51 inhibits p300-mediated H2B lysine acetylation and alters chromatin accessibility. Reversal of these inhibitory effects leads to enhanced p300-mediated histone acetylation and a gene expression program that favors oncogenic cell proliferation and tumor progression.

[See also Supplementary Figs. S17–S19]