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. 2017 Jul 28;7:6847. doi: 10.1038/s41598-017-07126-7

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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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The proposed model of regulation of DDR2 expression by a combination of c-Myb, LEF1, and p300 in lung cancer. The overall model following from the results of this study suggestive of the mechanism behind the regulation of DDR2 expression via p300 and transcription factors c-Myb and LEF1 under the influence of ECM stiffness. On a soft matrix, physical binding between c-Myb or LEF1 and DDR2 promoter is relatively weak. p300 expression is also weak, leading to lowered acetylation of c-Myb. Consequently, DDR2 promoter is not very active under the soft-matrix conditions; therefore, cellular proliferation and invasiveness are low. On the other hand, direct binding of c-Myb, LEF1, and the DDR2 promoter is significantly increased on a stiff matrix. p300 expression is also induced, resulting in increased acetylation of c-Myb, which enhances DDR2 promoter activity. Thus, DDR2 expression is increased under the stiff-matrix conditions, thereby increasing cellular proliferation and invasiveness.