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. 2017 Jul 21;7:6174. doi: 10.1038/s41598-017-06351-4

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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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BER is necessary for induction of AREG and EREG expression downstream of integrin α6β4 signaling. (A,B) RNA was isolated from Panc1-3D7 cells stably expressing non-targeting or shRNA specific for TET1. QPCR analysis was used to confirm TET1 knockdown (A) and expression of AREG and EREG (B). (C) Nuclei were isolated from Panc1-2G6, Panc1-3D7, and Panc1-3D7 cells expressing specific lentiviral shRNA for TDG. Western blot analysis was performed on nuclear fractions for TDG and Lamin A/C used as a loading control. (D) Cells were collected and AREG and EREG expression measured by QPCR. (E,F) Cells were treated with either 1 μM or 10 μM 3,4-Dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2 H)-isoquinolinone (DPQ) for 72 hours. Expression of AREG and EREG was measured by QPCR in Panc-2G6 (low α6β4; E) and Panc-3D7 (high α6β4; F) cell lines. Data depicted are representative of at least three different experiments and represent the mean +/− standard deviation. Statistical significance was calculated using a one-tailed t-test in which *denotes P < 0.05 as compared to controls.