EPHA2 Antibody - #AF5238

Figure 5 PTIP inhibits ESCC cell invasion and migration through EphA2. (A) Western blotting analysis against PTIP, EphA2, pS897-EphA2, pY588-EphA2 in PTIP knockdown(shPTIP#1, shPTIP#2) and control (shCtrl) TE1 cells. (B) IHC score for EphA2 in ESCC tumor sections. Unpaired, two-tailed Student’s t-test; **P < 0.01. (C) Representative IHC images for EphA2 in ESCC tumor sections. Low EphA2 and high EphA2 groups were divided based on the EphA2 immunostaining intensity scores mentioned in method. Cut off for high and low EphA2 expression in ESCC was defined < or > 11. (D) Percentage of invasion and non-invasion in ESCC groups. The differences between rates were tested by χ2; *P < 0.05. (E) Comparative expression between PTIP and EphA2 in ESCC samples from (B) analyzed by Pearson correlation. (F) Knockdown efficiency of shRNAs targeting PTIP and EphA2 in TE1 cells as determined by qRT-PCR. One-way ANOVA; *P < 0.05,**P < 0.01, ***P < 0.001. (G, H) The effect of PTIP and EphA2 double knockdown on the invasiveness of TE1 cells. For invasion assay, six different microscopic fields (magnification, ×10) from at least three independent experiments were examined; Relative intensities of the fields were measured (n ≥3). Representative images and statistical plots are shown; Mean ± s.d. are given for three independent experiments. One-way ANOVA; ***P <0.001. (I) ChIP-seq density profiles for PTIP in TE1 cells. Gene models are shown below the density profiles. (J, K) ChIP-qPCR primer sets marked with arrows were designed to cover regions present within (EphA2) or outside (EphA2-NC) of the EphA2 gene (C). ChIP-qPCR analyses of EphA2 binding (D). Representative images and statistical plots are shown; Mean ± s.d. are given for three independent experiments. Unpaired, two-tailed Student’s t-test; **P < 0.01.

Figure 5 PTIP inhibits ESCC cell invasion and migration through EphA2. (A) Western blotting analysis against PTIP, EphA2, pS897-EphA2, pY588-EphA2 in PTIP knockdown(shPTIP#1, shPTIP#2) and control (shCtrl) TE1 cells. (B) IHC score for EphA2 in ESCC tumor sections. Unpaired, two-tailed Student’s t-test; **P < 0.01. (C) Representative IHC images for EphA2 in ESCC tumor sections. Low EphA2 and high EphA2 groups were divided based on the EphA2 immunostaining intensity scores mentioned in method. Cut off for high and low EphA2 expression in ESCC was defined < or > 11. (D) Percentage of invasion and non-invasion in ESCC groups. The differences between rates were tested by χ2; *P < 0.05. (E) Comparative expression between PTIP and EphA2 in ESCC samples from (B) analyzed by Pearson correlation. (F) Knockdown efficiency of shRNAs targeting PTIP and EphA2 in TE1 cells as determined by qRT-PCR. One-way ANOVA; *P < 0.05,**P < 0.01, ***P < 0.001. (G, H) The effect of PTIP and EphA2 double knockdown on the invasiveness of TE1 cells. For invasion assay, six different microscopic fields (magnification, ×10) from at least three independent experiments were examined; Relative intensities of the fields were measured (n ≥3). Representative images and statistical plots are shown; Mean ± s.d. are given for three independent experiments. One-way ANOVA; ***P <0.001. (I) ChIP-seq density profiles for PTIP in TE1 cells. Gene models are shown below the density profiles. (J, K) ChIP-qPCR primer sets marked with arrows were designed to cover regions present within (EphA2) or outside (EphA2-NC) of the EphA2 gene (C). ChIP-qPCR analyses of EphA2 binding (D). Representative images and statistical plots are shown; Mean ± s.d. are given for three independent experiments. Unpaired, two-tailed Student’s t-test; **P < 0.01.

Fig. 1 The expression level of EphA2 protein in normal breast tissues, paracancerous tissues and breast cancer tissues as analyzed by immunofluorescence staining (A) and Western blotting (B).

Fig. 1 The expression level of EphA2 protein in normal breast tissues, paracancerous tissues and breast cancer tissues as analyzed by immunofluorescence staining (A) and Western blotting (B).