Fig. 2

Correlation of ARID1A and DUSP4 expression in mouse endometrial tissues and human uterine endometrioid carcinoma tissues. a A schematic presentation of the genetically engineered mouse models used in this study. The deletion of Arid1a and/or Pten in Pax8-expressing tissues (uterine epithelial cells) is achieved by activation of the Pax8 promoter via administration of doxycycline (see sect. “Materials and methods”). b Representative photomicrographs of Arid1a and Dusp4 immunoreactivity in iAD mice with (Dox +) or without (Dox−) doxycycline-induced Arid1a deletion. d Representative photomicrographs of Arid1a and Dusp4 immunoreactivity in iPD and iPAD mouse models in the presence of doxycycline-induced gene deletion. c H-score quantitation of DUSP4 expression in iAD, iPD, and iPAD mice. iAD mice: n = 7 for the Dox + group, n = 5 for the Dox- group; iPD mice, n = 6; iPAD mice: n = 6. e Representative photomicrographs of ARID1A and DUSP4 immunoreactivity from human uterine endometrioid carcinoma tissues. f H-score quantitation of DUSP4 immunoreactivity in human uterine endometrioid carcinoma tissues. iAD inducible Arid1a deletion, iPD inducible Pten deletion, iPAD inducible Arid1a and Pten deletion, Dox− mice did not receive doxycycline, Dox +  mice received doxycycline, ARID1A⁺ ARID1A retained, ARID1A⁻ ARID1A loss. A P < 0.05 was considered significant in (c) and (f)