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Fig. 1 | Molecular Cancer

Fig. 1

From: Disruption of ETV6 leads to TWIST1-dependent progression and resistance to epidermal growth factor receptor tyrosine kinase inhibitors in prostate cancer

Fig. 1

Twist1 is transcriptionally suppressed by Etv6. (a) Establishment of mouse prostate cancer cell lines (AC1, AC3, C1, and C2) from primary tumors of prostate-specific Pten/Tp53-null mice. (b) Monitoring of mRNA in a wild-type (WT) mouse prostatic basal cell line and four mouse prostate cancer cell lines. (c) Monitoring of mRNA in AC1 and AC3 prostate cell lines. (d) Left: Schematic of a predicted Etv6 response element (Etv6 RE) and a non-specific site (non-Etv6 RE) on the mouse Twist1 promoter. Right: Mouse Twist1-red fluorescent protein (RFP) reporter construct containing the WT or mutated ETV6 response element (WT vs. Mut), followed by the RFP. (e) ChIP analysis using an antibody (Ab) against the Etv6 protein at two RE sites (Etv6 vs. non-Etv6) in two mouse prostate cancer cell lines. An antibody against GAPDH at Etv6 RE served as a nonspecific control. The signal was determined as a percentage of the total input and was then normalized to immunoglobulin G (IgG). (f) ChIP analysis in response to Etv6 knockdown (siEtv6). scr., control siRNA. (g, h) Twist1-RFP reporter assay. The signal of the reporter construct containing either a WT or Mut Etv6 RE was measured in response to Etv6-knockdown (scr. vs. siEtv6, panel g) or Etv6 expression by transient transfection (EV vs. Etv6, panel h). EV, control vector. Quantification of mRNA was normalized to Gapdh, and results are presented as the mean ± SEM, n = 3. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, non-significant

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