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Fig. 4. ABI2 deficiency causes EMT and increases phosphorylation of ABL1 kinase tyrosine 412. (A) Effect of ABI2 expression on EMT markers. (B) Effect of ABI2 expression on cell motility and invasiveness. (C) Effect of ABI2 expression on ABL1 phosphorylation. (D) Effect of PRR16 expression on ABL1 phosphorylation. (E) Mechanism of action of PRR16 via interaction with ABI2 in EMT. MCF7 and SK-BR-3 cells were transfected with siRNA to inhibit ABI2. MCF7 and SK-BR-3 cells were transfected with plasmid DNA to overexpress PRR16, while MDA-MB-231 cells were transfected with siRNA to decrease PRR16 expression. The protein level were validated using Western blot. Cell migration and invasiveness were assessed using fibronectin-coated transwell assay and the Matrigel-coated transwell assay, respectively. Data are presented as the mean ± SD of three to four independent experiments. **p<0.01; ***p<0.001 in comparisons between the indicated groups using a Student’s t-test.
Biomolecules & Therapeutics 2022;30:340~347 https://doi.org/10.4062/biomolther.2022.066
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