Iron chelator stabilized IL-8 mRNA through activation of p38 and ERK1/2

<p><b>Copyright information:</b></p><p>Taken from "Differential regulation of iron chelator-induced IL-8 synthesis via MAP kinase and NF-κB in immortalized and malignant oral keratinocytes"</p><p>http://www.biomedcentral.com/1471-2407/7/176</p><p>BMC Cancer 2007;7():176-176.</p><p>Published online 13 Sep 2007</p><p>PMCID:PMC2078595.</p><p></p> IHOK and HN12 cells were treated with DFO (1.0 mM) for 16 h to allow accumulation of IL-8 mRNA. Cells were then treated with the mRNA synthesis inhibitor actinomycin D (ActD; 5 μg/ml), and either ERK pathway inhibitor (PD98059) or p38 inhibitor (SB203580). GAPDH mRNA was used as an endogenous control message. Same procedure as described in the legend to Fig. 1 was performed. Results are representative of three independent experiments

Iron chelator induces IL-8 protein secretion (A, C) and IL-8 mRNA accumulation (B, D) in IHOK and HN12 cells in a time-dependent manner

<p><b>Copyright information:</b></p><p>Taken from "Differential regulation of iron chelator-induced IL-8 synthesis via MAP kinase and NF-κB in immortalized and malignant oral keratinocytes"</p><p>http://www.biomedcentral.com/1471-2407/7/176</p><p>BMC Cancer 2007;7():176-176.</p><p>Published online 13 Sep 2007</p><p>PMCID:PMC2078595.</p><p></p> Cells were incubated with DFO (1.0 mM) or IL1-β (10 ng/ml) for the indicated time periods. Levels of IL-8 protein and mRNA were determined by ELISA and semiquantitative RT-PCR, respectively. Numbers below the gels represent the intensity of IL-8 mRNA relative to GAPDH mRNA. These data are representative of three independent experiments

The effect of inhibitor for p38 and ERK MAPK on iron chelator induced IL-8 protein secretion and IL-8 mRNA in IHOK and HN12 cells

<p><b>Copyright information:</b></p><p>Taken from "Differential regulation of iron chelator-induced IL-8 synthesis via MAP kinase and NF-κB in immortalized and malignant oral keratinocytes"</p><p>http://www.biomedcentral.com/1471-2407/7/176</p><p>BMC Cancer 2007;7():176-176.</p><p>Published online 13 Sep 2007</p><p>PMCID:PMC2078595.</p><p></p> IHOK (A) & HN12 cells (C) were pretreated with ERK inhibitor PD98059 and the p38 inhibitor SB203580 for 1 h and followed by the treatment with DFO (1.0 mM) for 16 h. Levels of IL-8 secretion and IL-8 mRNA were determined by ELISA and RT-PCR in IHOK (B) & HN12 cells (D). Same procedure as described in the legend to Fig. 1 was performed. Results are expressed as means ± SD of three independent experiments. *: Statistically significant difference compared to control group: p < 0.05, #: Statistically significant difference compared to DFO group, < 0.05

Iron chelator induced phosphorylated IκB-α in IHOK and HN12 cells on time dependent

<p><b>Copyright information:</b></p><p>Taken from "Differential regulation of iron chelator-induced IL-8 synthesis via MAP kinase and NF-κB in immortalized and malignant oral keratinocytes"</p><p>http://www.biomedcentral.com/1471-2407/7/176</p><p>BMC Cancer 2007;7():176-176.</p><p>Published online 13 Sep 2007</p><p>PMCID:PMC2078595.</p><p></p> Cells were treated with DFO (1.0 mM) or IL-1α (10 ng/ml) for the indicated time periods. Levels of IκB-α, p IκB-α were determined by Western blotting. The protein fraction was extracted, electrophoresed, transferred to membrane and blotted with respective antibodies. These data are representative of three independent experiments