Skip to main content
. 2014 Dec 23;106(1):78–85. doi: 10.1111/cas.12574

Figure 2.

Figure 2

Irradiation promotes epithelial–mesenchymal transition (EMT) through activation of SRC in breast cancer cells. (a) Kinase assay for SFK proteins (SRC, LYN, FYN, and LCK) using enolase as a substrate in MCF7 breast cancer cells after exposure to fractionated radiation. (b) Migration and invasion assay in MCF7 cancer cells transfected with siRNA targeting SRC or scrambled control siRNA (si-Cont) prior to irradiation. (c, d) Western blot analysis (c) and immunocytochemistry (d) for EMT markers E-cadherin, N-cadherin, and vimentin in MCF7 cancer cells transfected with siRNA targeting SRC or scrambled control siRNA prior to irradiation. (e, f) Western blot analysis for EMT transcription factors SLUG, SNAIL, ZEB1, and TWIST (e), and immunocytochemistry for EMT transcription factor SLUG (f) in MCF7 cancer cells transfected with siRNA targeting SRC or scrambled control siRNA prior to irradiation. (g, h) Migration and invasion assay in MCF7 (g) and SKBR3 (h) cancer cells transfected with SRC WT, mutant form SRC Y527F, or control vector pcDNA3.1. (i) Western blot analysis for E-cadherin and N-cadherin in MCF7 cells transfected with SRC WT, mutant form SRC Y527F, or control vector pcDNA3.1. β-actin was used as a loading control. Error bars represent mean ± SD of triplicate samples. *P < 0.05; **P < 0.01. Cont, control; IP, Immunoprecipitation.