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. 2019 Aug 12;9:11661. doi: 10.1038/s41598-019-48152-x

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© The Author(s) 2019

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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Pharmacological targeting of SMARCA4 impairs proliferation of SMARCA2-deficient ESCC KYSE-30 cells. (A) Schematic representation of siRNA/sgRNA-resistant SMARCA4 variant with substituted BRD9 bromodomain (SMARCA4^res-BD^BRD9). KYSE-30 cells were stably transduced with SMARCA4^res-BD^BRD9 followed by knock-out of endogenous SMARCA4 and generation of a monoclonal cell line (KYSE-30-SMARCA4^res-BD^BRD9). (B) Capillary Western immunoassay for SMARCA4 in parental KYSE-30 and KYSE-30-SMARCA4^res-BD^BRD9 upon dBRD9 treatment for 4 h with the indicated doses. GAPDH expression was used to monitor equal loading. Quantification of SMARCA4 expression (lower panel) is represented as mean ± SD of four independent experiments. (C) Cell viability assay. Parental KYSE-30 cells and KYSE-30-SMARCA4^res-BD^BRD9 were treated as indicated with dBRD9 and cell viability was determined ten days post treatment. Data are represented as mean ± SD of four independent experiments.