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Fig. 1 | Breast Cancer Research

Fig. 1

From: SETDB1 interactions with PELP1 contributes to breast cancer endocrine therapy resistance

Fig. 1

SETDB1 regulates ER driven transcription. A, B Expression level of SETDB1 between normal and BC tumor (A), and BC subtypes (B) were examined using online platforms TNM plot (A) and UALCAN portal (B). C Validation of SETDB1-KD by Western blotting using two independent shRNAs targeting SETDB1 in ZR75 and MCF7 cells. D Effect of SETDB1 KD on the cell viability of ER+ BC cells cultured in E2 (10−8 M) was measured by MTT assay. E MCF7 control-sh and SETDB1-sh cells were stimulated with E2 (10−8 M) for 8 h and then subjected to RNA-seq. Volcano plot of differentially expressed genes from RNA-seq data of MCF7 control-sh and SETDB1-sh cells. The x axis shows the log2 fold change and the y-axis shows the − log10 (p.value). The red dots represent significantly upregulated genes whereas the blue dots represent significantly downregulated genes upon SETDB1-KD. F GSEA enrichment plots of estrogen response signaling genes altered with SETDB1-KD. NES, normalized enrichment score. p values and FDR q.values were calculated using the GSEA package. G Representative KEGG pathways enriched (p.value < 0.05) in genes down-regulated upon SETDB1-KD. H 293 T-ERα-ERE-Luc cells were co-transfected with SETDB1 expressing vector or control vector along with pRL vector. After 48 h cells were stimulated with E2 for 24 h and luciferase activity was determined using Renilla dual luciferase assay system. I MCF7 cells that stably express SETDB1-shRNA were transduced with ERE-Luc, stimulated with E2 for 24 h and the reporter activity was determined. J Heat map depicting the expression levels of ER target genes from RNA-seq. K Selective ER target genes were validated by RT-qPCR in MCF7 control-sh and SETDB1-sh cells. Data was represented as mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001

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