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. 2017 Nov 16;7:15683. doi: 10.1038/s41598-017-15979-1

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© The Author(s) 2017

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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TNF-α induces KLF5 expression via the p38 pathway in cervical cancer cells. (a) Erk, Akt and p38 MAPK phosphorylation in HeLa cells was analysed by western blotting. β-actin was used as the loading control. (b) The activation levels of these three kinases were determined by the respective phosphorylation ratios. *P < 0.05, **P < 0.01. (c) The cellular locations of KLF5 (red) and tumour necrosis factor receptor superfamily member 11a (TNFRSF11a, green) in HeLa cells were determined by immunofluorescence staining (×200). DAPI was used for nuclear staining. Scale bars = 10 μm. (d) Statistical analysis of fluorescence intensity. *P < 0.05 vs. the TNF-α group. KLF5 expression in HeLa cells was determined at the protein (e) and mRNA levels (f). *P < 0.05 vs. the TNF-α group.