Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

Skip to main content
Fig. 3 | Journal of Biomedical Science

Fig. 3

From: Metformin sensitizes triple-negative breast cancer to histone deacetylase inhibitors by targeting FGFR4

Fig. 3

Metformin reversed SAHA-induced feedback activation by inhibiting histone acetylation on FGFR4. A The Venn diagram displayed the intersection of upregulated genes in the SAHA-treated group, downregulated genes in the Metformin-treated group, downregulated genes in the SAHA + Metformin combination group, and membrane receptor genes. B GSEA analysis was performed on the differential expression results between the SAHA-treated group and the control group. C Immunoblotting showed the change in FGFR4 and STAT3 phosphorylation. MDA-MB-231 cells pretreated with JQ1 for 24 h were exposed to SAHA for a further 12 h. FGFR4 and STAT3 phosphorylation changes were detected by immunoblotting. All bands were quantified from experiments repeated three times. D Histone acetylation on the FGFR4 promoter. (Left) MDA-MB-231 cells were treated with SAHA (5 μM) for 12 h before being subjected to ChIP assay using anti-acetylhistone H3K9 (Ac-H3K9) antibody followed by qPCR analysis using primers targeting the indicated FGFR4 promoter region. (Middle) BRD4 enrichment on the FGFR4 promoter. MDA-MB-231 cells were treated with SAHA (5 μM) for 12 h before being subjected to ChIP assay using anti-BRD4 antibody. qPCR analysis was performed using primers targeting the indicated FGFR4 promoter region. (Right) MDA-MB-231 cells were treated with Metformin (20 mM) for 48 h before being subjected to ChIP assay using anti-acetylhistone H3K9 (Ac-H3K9) antibody followed by qPCR analysis using primers targeting the indicated FGFR4 promoter region. All experiments were performed in triplicate. Error bars represent means ± SD from triplicates. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. E FGFR4 mRNA level changes. MDA-MB-231, BT-549, and HCC1806 cells were treated with SAHA (5 μM) for 24 h or metformin (20 mM) for 48 h. Samples were analyzed by qPCR assay. Error bars represent means ± SD from triplicates. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. F Immunoblotting showed the change in FGFR4 and STAT3 phosphorylation. (Left) MDA-MB-231 cells were treated with indicated SAHA (0, 5, 10 μM) for 12 h. (Middle) MDA-MB-231 cells were treated with indicated metformin (0, 10, 20, 40 mM) for 48 h. (Right) MDA-MB-231 cells pretreated with metformin (20 mM) for 36 h were exposed to SAHA (5 μM) for further hours. FGFR4 and STAT3 phosphorylation changes were detected by immunoblotting. All bands were quantified from experiments repeated three times

Back to article page