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Fig. 7 | Breast Cancer Research

Fig. 7

From: Methylglyoxal, a glycolysis metabolite, triggers metastasis through MEK/ERK/SMAD1 pathway activation in breast cancer

Fig. 7

Methylglyoxal (MG)-related invasive phenotype is associated with a decrease in DUSP5 phosphatase expression in breast cancer cells. a Dual specificity phosphate (DUSP)1, 5, 8, 10, 12, 14 and 16 phosphatase messenger RNA (mRNA) levels in glyoxalase 1 (GLO1)-depleted MDA-MB-231 cells were quantified by qRT-PCR. b DUSP5 and DUSP8 protein expression in MDA-MB-231 and MDA-MB-468 shGLO1 cells cultured in serum-free medium for 24 h was assessed using immunoblot. DUSP5 mRNA (c) and protein (d) levels in MDA-MB-231 and MDA-MB-468 cells, respectively, treated with MG at the indicated concentrations for 3 h in serum-free medium. e and f DUSP5, (P-)extracellular signal-related protein kinase (ERK) and (P-)SMAD1 (ser206) protein levels were assessed using immunoblot in GLO1-silenced MDA-MB-231 and MDA-MB-468 cells upon DUSP5 overexpression, respectively. Immunoblots were quantified by densitometric analysis and normalized for β-actin. Numbers represent fold increase relative to the condition shown with bold number. All western blots are representative of three independent experiments. g, h Quantification of migration assays of MDA-MB-231 and MDA-MB-468 shGLO1 cells upon DUSP5 overexpression, respectively. Data were analyzed using one-way analysis of variance (ANOVA) followed by Dunnett post-hoc test or two-way ANOVA followed by Bonferroni post-hoc test and are shown as mean values ± SEM of three independent experiments. ns, not significant; *p < 0.05, **p < 0.01 and ***p < 0.001. i Key biological processes (green boxes) and regulatory pathways (yellow boxes) by which MG stress contributes to the metastatic phenotype. For the sake of clarity, the regulation of genes of the pro-metastatic signature exerted through the inhibition of MEK/ERK pathway (U0126 inhibitor) and SMAD1 (siSMAD1) is not represented (please see “Results” section for details)

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