Abstract:
Objective: To investigate the interaction between Smad1 and estrogen in the promotion of breast cancer, as well as its functional role and underlying mechanism.
Methods: The interaction relationship of Smad1 and estrogen was detected by Western blotting and real-time PCR. Smad1 was down-regulated using short hairpin RNA (shRNA) interference technology in breast cancer cells. Using Transwell method, IHC and cell counting method to observe the effect of Smad1 on cell proliferation and invasion.
Results: Smad1 could increase transcription and translation of breast cancer cells in the stimulation of estrogen. p-Smad1 was activated after four hour activation of estrogen and then reach maximum at twelve hour later (
P< 0.001). The expression of Smad1 in cancer tissue was enhanced compared to paratumor tissues and Smad1 level was positively correlated with ERα while p-Smad1 activation was inhibited.
In vitro cell proliferation, RNA interference silencing of Smad1 in two breast cancer cells decreased propagation ability significantly (
P< 0.05);
in vivo tests, tumor growth was also significantly inhibited (
P< 0.05).
Conclusions: The study indicates estrogen manipulation in breast cancer cells depending on Smad1. BMP-Smad1 pathway plays complex controlling role in the process of cell occurrence and development.