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. 2022 May 12;13:2642. doi: 10.1038/s41467-022-30375-8

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© The Author(s) 2022

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. 3 — a Immunoblot analysis of CDK12 expression in MCF10A cells stably transfected with CDK12 (CDK12-OE) or empty vector control (EV), and in CDK12-amplified BT474 breast cancer cells. Vinculin (Vinc.), loading control. b Growth kinetics of CDK12-OE vs. EV MCF10A cells in 2-D culture. Data are means ± SEM (n = 3). **P = 0.002, ***P < 0.001, two-sided unpaired t-test. c Typical morphological appearance of 3D-acini generated by CDK12-OE vs. EV MCF10A cells cultivated in Matrigel for 18 days. Left panels in each condition are magnified on the right to better show the hollowed vs. filled/disorganized/branched structures of EV vs. CDK12-OE MCF10A cells, respectively. Bar, 100 μm. d Quantitation of the experiment in (c). Data are means ± SD (n = 5). ***P < 0.001, two-sided unpaired t-test.