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. 2017 Aug 28;1(8):816–830. doi: 10.1002/hep4.1086

Figure 8.

Figure 8

Schematics summarizing major findings in the present study. HMGB2 is critical to maintain the pluripotent state of mouse ESCs. HMGB2 enhances OCT4/SOX2 transcriptional activity by binding to OCT4 and increasing OCT4 and SOX2 protein expression. Down‐regulation of HMGB2 protein by ICM disrupts stem cell polarity and impacts normal EB formation. miR‐127 functions as a new repressor of HMGB2 protein expression by inhibiting HMGB2 3'UTR activity and HMGB2 mRNA translation. SHP serves as a new transcriptional repressor of HMGB2 mRNA expression by inhibiting the promotor activity of HMGB2 through E2F1. Overexpression of miR‐127 or SHP facilitates germ layer differentiation by diminishing HMGB2 expression. The induction of HMGB2 in TICs as well as in various human cancers suggests its potential oncogenic function. This effect could be mediated through regulating cancer stem cells, which will be elucidated in future studies (question mark). Overall, our study unravels a crosstalk between HMGB2 and miR‐127/SHP to control mouse ESC differentiation.