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. 2020 May 8;10:7826. doi: 10.1038/s41598-020-64832-5

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Effect of ERK MAPK inhibition on COX2 expression and PGE₂ production. Protein levels in whole cell lysates were detected by Western blotting with Actin as loading control. Amount of PGE₂ in culture medium was measured by enzyme-linked immunosorbent assay and normalised to cell number. Bar graph represents % control of PGE₂ production. (A) cUC cells (Sora) were treated with vehicle (dimethyl sulfoxide; Cont) and inhibitors of BRAF (Dabrafenib; Dab), pan-RAF (LY3009120; LY), MEK (PD0325901; PD) and ERK (SCH772984; SCH) at 1 μM for indicated time. (B) cUC cells (Sora) were treated with vehicle (Cont), Dabrafenib (Dab), LY3009120 (LY), PD0325901 (PD) and SCH772984 (SCH) for 12 h at indicated dose. (C) cUC cell lines (TCCUB, Love, Nene, NMTCC, LTCC, MCTCC and OMTCC) were treated with vehicle (Cont), Dabrafenib (Dab) at 10 μM, LY3009120 (LY) at 1 μM, PD0325901 (PD) at 10 μM and SCH772984 (SCH) at 10 μM for 12 h. Data are presented as mean ± SD of three experiments. *Indicates p < 0.05, **p < 0.01, ^‡p < 0.001 compared to vehicle control (Dunnett’s test).