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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: Interruption of the long non-coding RNA HOTAIR signaling axis ameliorates chemotherapy-induced cachexia in bladder cancer

Fig. 2

Cisplatin treatment upregulates HOTAIR through the EGFR-ProT axis in bladder cancer cells. a Cisplatin treatment activates EGFR and NF-κB and promotes ProT expression. Detection and quantitation of EGFR and its phosphorylated form (p-EGFR), NF-κB p65 and its phosphorylated form (p-NF-κB p65), as well as ProT in J82 cells treated with indicated concentrations of cisplatin (0 to 2 μg/ml) for 48 h by immunoblot analysis. b, c Cisplatin treatment activates NF-κB and promotes ProT and HOTAIR expression through the EGFR signaling pathway. J82 cells were treated with cisplatin (2 μg/ml) for 24 h followed by addition of gefitinib (10 μM), erlotinib (1 μM), or the vehicle (DMSO) for an additional 24 h. d, e Cisplatin treatment upregulates HOTAIR through ProT. J82 cells that had been transduced with or without lentiviral vectors expressing shRNA specific for human ProT (#17 and #19) or luciferase (Luc) were treated with cisplatin (2 μg/ml) for 48 h. Expression of ProT as well as NF-κB p65 and its phosphorylated form was examined by immunoblot analysis (n = 3) (b, d), and HOTAIR was quantified by RT-qPCR (n = 4) (c, e). Expression of β-actin served as the loading control for immunoblotting. Representative immunoblots from three independent experiments and quantitative analysis of the indicated proteins are shown (a, b, d). Values shown are mean ± SD (n = 4). The ratios of control cells were arbitrarily set to 100

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