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. 2018 Jan 24;12(3):305–321. doi: 10.1002/1878-0261.12162

Figure 6.

Figure 6

Double inhibition of Sp1 and Smad3 significantly affects the TGF‐β‐induced increase in EGFR expression. (A) Inhibition of Sp1 by MTM in Smad3‐silenced cells showed a significant decrease in the mRNA expression of EGFR. Smad3‐knockdown cells were treated with or without MTM and then stimulated with TGF‐β for 24 h. The expression of EGFR mRNA was analyzed by qRT‐PCR. Statistical analysis was carried out by two‐way ANOVA (*P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001). (B) Western blot analysis showed that the TGF‐β‐induced EGFR protein level in MTM‐treated Smad3‐knockdown cells was significantly lower than that of the control or Smad3‐silenced cells. (C) Double knockdown of Sp1 and Smad3 in breast cancer cells showed more strong inhibition of TGF‐β‐induced upregulation of EGFR expression than that in the single‐Sp1 and single‐Smad3 siRNA‐transfected breast cancer cells. Moreover, Sp1‐knockdown cells showed much stronger inhibitory effect on TGF‐β‐induced EGFR upregulation compared to Smad3‐knockdown cells. (D) A proposed schematic model: TGF‐β transactivates EGFR and promotes migration and invasion abilities of breast cancer cells.