Author(s)

Pan Hongming, Sun Lihui, Zhang Haiyan, Li Lin, Lian Jie, Yujing, Lang Weiya

Corresponding Author

Lang Weiya

Abstract

objective: to investigate the effect of trichostatin a (tsa) on the migration and invasion of breast cancer mda-mb-231 and its possible molecular mechanism. Methods: mda-mb-231 cells were cultured in vitro until the logarithmic growth period, and treated with tsa at different concentrations of 20, 40, 80 and 160 nmol / l for 72 hours. Cell viability was detected by cck-8, apoptosis was detected by flow cytometry, migration and invasion were detected by scratch test and transwell cell. Western blotting was used to detect the protein levels of mmp-2, mmp-9, p-erk, p-jnk and p38 mapk. Results: tsa could inhibit the activity of mda-mb-231 cells in a dose-dependent manner (p < 0.05); tsa could inhibit the migration and invasion of mda-mb-231 cells in a dose-dependent manner (p < 0.05). Western blotting results showed that tsa down-regulated mmp-2 and mmp-9 protein expression levels, and up-regulated p-p38 mapk and e-cadherin protein expression levels (p <0.05). Tsa had no significant effect on p-erk and p-jnk protein expression levels, and the difference was not statistically significant (p> 0.05). After p38 mapk inhibitor sb203580 combined with tsa, the cell scratch healing rate increased and the proliferation activity increased with the increase of mmp-2 and mmp-9 protein expression levels, and the decrease of e-cadherin protein expression levels. <0.05). Conclusion: tsa can migrate and invade breast cancer mda-mb-231 cells. It down-regulates mapk / p38 signaling pathway, mmp-2 and mmp-9 protein expression, and up-regulates e-cadherin protein expression.

Keywords

Trichostatin a; Breast Cancer; Migration and Invasion; Signal Pathway