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. 2022 Mar 17;21:15347354221086900. doi: 10.1177/15347354221086900

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© The Author(s) 2022

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — The inhibitory effect of hesperetin on the activation of Fyn and phosphorylation of paxillin in MDA-MB-231 breast cancer cells. (A and B) Hesperetin inhibited the activation of Fyn in MDA-MB-231 cells. (A) Analysis of Fyn activation via p-Src immunoblotting after Fyn immunoprecipitation from MDA-MB-231 cell samples. Representative western blot showed the variation of p-Src (Y420) in different groups. (B) Statistical analysis revealed that Fyn activation (proportion of Fyn phosphorylation at Y420 to total Fyn after Fyn immunoprecipitation). Data were presented as the mean ± SD, n = 6. *P < 0.05 versus control group; #P < 0.05 versus TGF-β1 group. (C–F) Hesperetin inhibited the tyrosine phosphorylation of paxillin at Y31, Y88, and Y118 sites induced by TGF-β1 in MDA-MB-231 cells. (C) The tyrosine phosphorylation of paxillin in MDA-MB-231 cells was analyzed by western blot. (D–F) Statistical analysis revealed tyrosine phosphorylation of paxillin (proportion of paxillin phosphorylation at Y31, Y88, and Y118 sites to total paxillin, respectively). Total paxillin was used as control. Data are expressed as the mean ± SD, n = 6. **P < 0.01 versus control group; ##P < 0.01 versus TGF-β1 group.