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. 2021 Oct 21;11:20775. doi: 10.1038/s41598-021-00231-8

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© The Author(s) 2021

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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The JAK1 tyrosine kinase controls the oncogenic activation of STAT3 in KRAS-induced mammary cancer cells. (A) PCR assays to validate the MMTV-Flp-mediated activation of the FSF-Kras^G12D allele (upper panel) and the Rosa26^{CAG-FSF-CreERT2} allele (lower panel) in mammary tumor cells from MMTV-Flp FSF-Kras^G12D Rosa26^{CAG-FSF-CreERT2} Jak1^fl/fl females. DNA from the tail of a mammary tumor-bearing animal was used as a control (upper panel). DNA from cells of a Pdx-Flp-induced pancreatic cancer that carried the Rosa26^{CAG-FSF-CreERT2} allele was used as a positive control (PC) for the FSF recombination in the Cre^ERT2 allele; NC no DNA, S DNA size markers. (B) Upper panel: PCR to determine the Flp-mediated deletion of the frt-flanked neomycin selection cassette in the Jak1 conditional knockout alleles of the tumor cells shown in (A). Lower panel: PCR assay to assess the Cre^ERT2-mediated deletion of the second coding exon of Jak1 before and after treatment with tamoxifen (Tam). DNA from MEFs with defined Flp and Cre-mediated deletions were used as positive controls (PC), and tail DNA from panel A served as negative control (NC). (C) Western blot analysis of mammary tumor cells before and after treatment with Tam to assess the effects of a Cre^ERT2-mediated deletion of JAK1 on STAT3 activation. GAPDH served as a loading control. A pair of isogenic cells from ERBB2-induced mammary tumors with JAK1 (PC) and without JAK1 (NC) was used as controls. (D) Immunofluorescent staining of pSTAT3 in histological sections of secondary mammary tumors that resulted from the transplantation MMTV-Flp FSF-Kras^G12D Rosa26^{CAG-FSF-CreERT2} Jak1^fl/fl mammary tumor cells and treatment with or without Tam.