Figure 2

<div><p><b>EZH2-mediated H3K27me3 was involved in epigenetic repression of DLC1 in HCC</b> and <b>multiple other human cancers.</b></p> <p>(<b>A</b>) DLC1 was transcriptionally induced upon stable knockdown of EZH2 in MHCC97L cells. (<b>B</b>) qChIP analysis confirmed the depletion of H3K27me3 enrichment on DLC1 promoter upon EZH2 knockdown in MHCC97L cells. Data are represented as mean ± SEM from three independent experiments. (<b>C</b>) DLC1 was transcriptionally repressed in Huh7 cells after transient overexpression of GFP-EZH2. (<b>D</b>) qChIP analysis revealed a concomitant enrichment of EZH2 at DLC1’s promoter locus upon GFP-EZH2 overexpression in Huh7 cells. Data are represented as mean ± SEM from three independent experiments. (<b>E</b>) EZH2 and H3K27me3 expression was reduced upon 1µM DZNep treatment for 48 hours in MHCC97L cells (left panel). DMSO was used as mock treatment. Pan H3 and α-tubulin were loading control of the immunoblot. DZNep treatment transcriptionally induced DLC1 expression in MHCC97L as indicated by qPCR analysis (right panel). (<b>F</b>) Different human cancer cells, including the nasopharyngeal carcinoma cell line CNE2, the colorectal carcinoma cell line HCT116 and the cervical adenocarcinoma cell line HeLa were examined for DLC1 re-expression upon DZNep treatment. Treatment of cells with 10µM DZNep reactivated DLC1 expression. <i>P</i>-values obtained from <i>t</i>-test.</p>