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. 2022 Oct 24;7(20):e157502. doi: 10.1172/jci.insight.157502

Figure 1. PRC2 deletion drives MPNST metastatic phenotypes in vitro.

Figure 1

(A) The 4 parental cell lines were derived from primary mouse MPNST models generated from either NC tumors (Nf1fl/fl Cdkn2afl/fl) mice injected with adenovirus expressing Cre recombinaseinto the sciatic nerve) or NP tumors (wild-type mice injected with adenovirus containing Cas9 and guide RNAs for Nf1 and p53 into the sciatic nerve). Isogenic panels were made by CRISPR editing of cells in vitro with Cas9 and guide RNAs targeting Eed, Suz12, or a nontargeting control (NT). (B) Representative Western blots of isogenic cell series show loss of EED, SUZ12, and the downstream functional target H3K27me3 compared with NT (n = 3). (C) Transwell migration assays show increased migration of ΔEed and ΔSuz12 cells compared with NT by 1-way ANOVA with Tukey’s multiple comparisons (n = 4). (D) Transwell invasion assays show increased invasion through collagen of ΔEed and ΔSuz12 cells compared with NT by Kruskal-Wallis with multiple comparisons (n = 3–6). Data represent biological replicates with the mean ± SD; *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.