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. 2020 Oct 27;10:18316. doi: 10.1038/s41598-020-75529-0

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Akt1 loss primarily increase thyroid cell apoptosis and reduces cell motility. Thyroid cell proliferation and apoptosis in vivo were examined by IHC using antibodies against Ki67 (A; n = 7 for all genotypes) and cleaved caspase-3 (B; n = 5 for all genotypes), respectively. Ki67 was not changed for the any of the KO mice. An increase in apoptosis was identified in the PVPV-Akt1KO thyroid glands vs PVPV-AktWT (*p = 0.008). There was a trend for an increase in PVPV-AKT2KO thyroid glands (p = 0.06). Cell migration (C) and invasion (D) of primary cultured thyroid cells in vitro were examined using Boyden chambers without or with Matrigel. PVPV-Akt1KO cells had reduced migration and PVPV-Akt1 and Akt3KO cells had reduced invasion. Cells from at least five different thyroids of each genotype mouse were tested. *p < 0.01, **p < 0.005. Graph images were created using Graphpad Prism version 8.4.2 (https://graphad.com). IHC quantitation was performed using InForm software version 2.3.0, (https://www.perkinelmer.com/Content/LST_Software_Downloads/inFormUserManual_2_3_0_rev1.pdf).