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. 2020 Apr 29;39(22):4436–4449. doi: 10.1038/s41388-020-1299-z

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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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Fig. 5 — The effect of p63 knockdown on TGFβ- and EGF-induced AP-1 and EGFR pathway components. MCF10A MII (a, b) and HCC1954 (c) cells were transfected with non-targeting control (siNTC), p63 siRNA, or ΔNp63-specific siRNA, serum-starved for 16 h, stimulated for 6 h with 5 ng/ml TGFβ1 or untreated, and analyzed by immunoblotting. One of three experiments with similar results, is shown. d and e MCF10MII cells were treated as in (a), stimulated with TGFβ1 (5 ng/ml) for 1.5 h (d) or 6 h (e), or untreated, and analyzed by qRT-PCR analysis. Statistics were calculated using one-way analysis of variance (ANOVA). The data were further analyzed using Tukey’s multiple comparisons test. Results from three independent experiments are shown as mean ± SD; ns, not significant, *P < 0.05, **P < 0.01, and ***P < 0.001. f ChIP-qPCR showing p63 binding to the indicated gene loci in MCF10A MII cells. One of two independent experiments with similar results, is shown.