Figure 3. Persistent DNA damage in normal-looking part of the livers of the Sgo1<sup>−/+</sup> mice. (A) The DNA damage marker phospho-gamma-H2AX and p53.

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Figure 3. Persistent DNA damage in normal-looking part of the livers of the Sgo1<sup>−/+</sup> mice. (A) The DNA damage marker phospho-gamma-H2AX and p53 were expressed at higher levels in livers of 12-month-old Sgo1<sup>−/+</sup> mice. Based on IHC pictures, percentages of IHC-positive cells (black nuclear stain) are calculated. (*) indicates that the P value is statistically significant. (B) A senescence marker p16<sup>INK4A</sup> and an apoptosis pathway marker Bcl2 were expressed at higher in livers of Sgo1<sup>−/+</sup> mice. (C) Expression of p53, p16<sup>INK4A</sup>, and Bcl2 were age-dependent. Livers from 4-month-old Sgo1<sup>−/+</sup> mice were analyzed as in (A) and (B). Only the DNA damage marker p-H2AX showed a significant difference from the control in the younger Sgo1<sup>−/+</sup> mice, suggesting that persistent DNA damage is an upstream event of the differential expression of other markers. (D) Age diminished Sgo1 protein expression level in untreated wild type. Younger wild type (4 months; left five lanes) expressed higher amount of Sgo1. In older mice (12 months; right six lanes), Sgo1 expression diminished. Modification of loading control α–tubulin was altered. From: Tumor-promoting/progressing role of additional chromosome instability in hepatic carcinogenesis in Sgo1 (Shugoshin 1) haploinsufficient mice Carcinogenesis. 2015;36(4):429-440. doi:10.1093/carcin/bgv011 Carcinogenesis | © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com 1