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. 2020 Mar 10;52(3):461–472. doi: 10.1038/s12276-020-0387-z

Fig. 5. LncRNA NEAT1 recruits EZH2 to the LATS2 promoter and represses LATS2 expression.

Fig. 5

The interaction between lncRNA NEAT1 and EZH2 was verified by RIP assay. *p < 0.05 vs. the IgG group (a). The enrichment of EZH2 and H3K27me3 on the LATS2 promoter region determined by ChIP (b). The protein expression patterns of EZH2, H3K27me3, and LATS2 in response to overexpression or knockdown of EZH2 measured by western blot analysis (c). Quantification of protein expression in c (d). Control group, HL-7702 cells without treatment; oe-NC group, HL-7702 cells treated with oe-NC; sh-NC group, HL-7702 cells treated with sh-NC; oe-EZH2 group, HL-7702 cells treated with oe-EZH2; sh-EZH2 group, HL-7702 cells treated with sh-EZH2. Statistical data are described as mean ± standard deviation. One-way analysis of variance was used for comparisons among multiple groups, followed by Tukey’s post hoc test. The experiment was repeated three times independently. lncRNA NEAT1 long noncoding RNA nuclear-enriched abundant transcript 1, LATS2 large tumor-suppressor kinase 2, EZH2 enhancer of zeste homolog 2, NC negative control, RIP RNA immunoprecipitation, ChIP chromatin immunoprecipitation.