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. 2019 Nov 26;12:10213–10225. doi: 10.2147/OTT.S211973

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© 2019 Ding et al.

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Phosphorylation on Y228 is critical on inhibiting colon cancer progression. Y228 on p120-catenin was mutated into E (Y228E) to mimic phosphorylated residue and F (Y228F) to abolish phosphorylation function. (A) The proliferation process of SW480 cells is evaluated by CCK-8 assay, showing that Y228F attenuated the anticancer effect of p120-catenin. (B) Similarly, Matrigel-transwell results indicated that the invasion capacity was further enhanced after mutating Y into E, compared with wild type (WT) p120-catenin. (C) Transcription of RhoA downstream effectors, such as snail and c-myc, was further impaired in Y228E while rescued in Y228F, indicating the crucial role of Y228 phosphorylation in suppressing cancer progression. (D) Y228E stabilizes the p120-catenin-RhoA interaction while Y228F interrupts this interaction, compared with the wild type. Consistently, the GTP-RhoA and ROCK1 levels were lowest in Y228E group. In contrast, the E-cadherin showed a highest level in Y228E transcription group. *Indicates P<0.05 by One-way ANOVA t test.