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Figure 4 | BMC Cancer

Figure 4

From: Fenofibrate induces apoptosis of triple-negative breast cancer cells via activation of NF-κB pathway

Figure 4

Fenofibrate induces apoptosis via activation of NF-κB pathway in a PPAR-α independent way. GW6471 (5 μM), a PPAR-α specific inhibitor, did not provide protection from anti-proliferation (A) and apoptosis (B) induced by fenofibrate. Data represent the means ± SD of three independent experiments. (C) Fenofibrate induced nuclear accumulation of p65 accompanied by increasing the levels of p-IKKα/β and IKKα and decreasing the level of p-IκBα, but had no impact on IκBα. (D) PDTC (10nM), a specific inhibitor of NF-κB, efficiently inhibited the nuclear accumulation of p65 induced by fenofibrate. (E) Cell apoptosis induced by fenofibrate was significantly decreased by co-treatment with fenofibrate and 10nM PDTC (** indicates p < 0.01 relative to fenofibrate treatment group). Data represent the means ± SD of three independent experiments. (F) Exposure to fenofibrate triggered a decrease in p-Akt1 and p-Erk1/2, but had no effects on Akt1 and Erk1/2. TFIIB was detected as a loading control of nuclear proteins. β-actin was served as a loading control of cytoplasmic proteins and whole cell proteins. N.S. = No statistical significance. Feno = fenofibrate.

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