Fig. 4 | Nature Communications

Fig. 4

From: Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma

Fig. 4

BET proteins maintain the liposarcoma (LPS) malignancy and active transcription. a, b Effects of short hairpin RNA (shRNA)-mediated silencing of BRD2, BRD3, and BRD4 on a cell viability and b anchorage-independent growth of DDLPS and MLPS cells. Data are presented as mean ± SEM; n = 3. c–e Effects of shRNA-mediated silencing of BRD2, BRD3, and BRD4 in DDLPS cells on their c tumorigenic ability (n = 8) and distant metastatic potential (n = 7) to d lung and e liver. Arrows indicate tumor nodules in liver. One-way analysis of variance (ANOVA) was applied for a–c; Student’s t-test (two-tailed) was applied in d, e. f Effect of shRNA-mediated silencing of BRD2, BRD3, and BRD4 on tumorigenic ability of MLPS cells. Tumor-free survival of xenograft-bearing animals and tumor incidence were recorded as the endpoint of experiment. Log-rank test was applied for statistical analysis (n = 10). g Pie charts of BET proteins binding to cis-regulatory regions of the LPS141 genome. h Heatmaps for the ChIP-seq signals of indicated antibodies ± 2 kb from TSS in LPS141 cells. i Venn-diagram showing BET (+) genes defined by promoter-proximal occupancy of BET proteins. j Differential expression of BET (+) genes and BET (−) genes in LPS141 cells. Box plot indicates median value (center line), first and third quartiles (box limits), as well as minimum and maximum values (whiskers) after excluding outliers (dots). Wilcoxon signed-rank test was applied. k Metagene plots showing differential enrichment of BET proteins in SE and TE regions of LPS141 genome. *p < 0.05; **p < 0.01; ***p < 0.001. Source data are provided as a Source Data file

Back to article page