Fig. 5

Effects of IKK-β on PLA-induced MMP-9 expression in cervical cancer cells. a‒c SiHa (a), HeLa (b), and C-33A (c) cells were treated with 10 mM PLA for the indicated times, and the activation of IKK-β was then examined by Western blot analysis. d‒f SiHa (d), HeLa (e), and C-33A (f) cells were pretreated with 10 μM IMD0354 (IMD, an inhibitor of IKK-β) for 90 min and then stimulated with 10 mM PLA for an additional 24 h. The expression of MMP-9 was measured by Western blot analysis. g‒h HeLa (g) and C-33A (h) cells were pretreated with 10 μM PD (ERK1/2 inhibitor), LY (PI3K/Akt inhibitor), H89 (PKA inhibitor), or GF (the inhibitor of PKC) for 90 min and then stimulated with 10 mM PLA for another 24 h. The activation of IKK-β were examined by Western blot analysis. i, j HeLa (i) and C-33A (j) cells were pretreated with 10 μM PD, LY, H89, or GF for 90 min, and then stimulated with 10 mM PLA for another 24 h. The expression of MMP-9 were examined by Western blot analysis. GAPDH expression was evaluated as a loading control. One representative of three different experiments, for each of the analyses performed, is shown