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. 2018 May 14;37(34):4692–4710. doi: 10.1038/s41388-018-0273-5

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© The Author(s) 2018

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. 2 — KMT2C loss inhibits proliferation of ER+ cells. a–d Breast cancer cells stably expressing either shRenilla or shKMT2C were assayed for proliferation using the alamarBlue cell viability assay. Values correspond to the mean of six experimental replicates ± s.e.m. All cells are cultured in full serum containing media e. Parental and MCF7 KMT2C CRISPR cells were assayed for proliferation using the alamarBlue cell viability assay. Values correspond to the mean of six experimental replicates ± s.e.m. Data correspond to one representative assay from a total of two or three independent assays. f–i Indicated breast cancer cells stably expressing either shRenilla, shKMT2C or shKMT2D were assayed for proliferation using the alamarBlue cell viability assay. Values correspond to the mean of six experimental replicates ± s.e.m.