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. 2015 Aug 10;6(30):29637–29650. doi: 10.18632/oncotarget.4936

Figure 6. COX-2 in TAMs enhanced the activation of PI3K/Akt pathway in breast cancer cells.

Figure 6

A. The activation of Akt in breast cancer cells co-cultured with or without TAMs transfected with adenoviral COX-2 or siRNA COX-2 was detected by Western blot. B. and C. Inhibiting Akt1 in breast cancer cells attenuated cell proliferation and drug resistance induced by COX-2 in TAMs. Breast cancer cells transfected with adenoviral siRNA Akt1 or Akt1 were co-cultured with or without TAMs transfected with adenoviral COX-2 or siRNA COX-2. Cell proliferation (B) and cell apoptosis (C) induced by ADM were measured by CCK-8 kit and flow cytometry, respectively. D. Inhibiting Akt1 resulted in the suppression of Bcl-2, P-gp and COX-2, and increase of Bax expression in breast cancer cells co-cultured with COX-2+ TAMs. The expression of related proteins in breast cancer cells was detected by Western blot. β-actin was used as an internal loading control, and the blots shown are representative of six independent experiments.