Fig. 5: STAT3/cJun/p27 co-repress PTPN12 in complex with YY1, SIN3A, and HDAC1. | Nature Communications

Fig. 5: STAT3/cJun/p27 co-repress PTPN12 in complex with YY1, SIN3A, and HDAC1.

From: C-terminally phosphorylated p27 activates self-renewal driver genes to program cancer stem cell expansion, mammary hyperplasia and cancer

Fig. 5

a Volcano plot of genes differentially expressed in 231DD vs. 231. b PTPN12 mRNA expression by qPCR in the indicated lines. c Western shows effects of p27CK-DD on total and activated STAT3 and Pyk2 and effects of PYK2 loss on STAT3 levels and STAT3pY705. d Western shows effects of p27pT198 (reduced by PI3K inhibitor, PF1502) and Pyk2 loss (siPYK2) and Pyk2 inhibition by PF431396 on STAT3 levels and activation (STAT3pY705) e p27, STAT3, and cJun co-occupied peaks at +2 kb of the PTPN12 TSS. f–k ChIP-qPCR shows p27 (f); STAT3 (g); cJun (h); SIN3A (i); YY1 (j) and HDAC1 (k) binding at +2 kb of the PTPN12 TSS where p27 peaks overlap with binding peaks of STAT3 and cJun. l cJun ChIP-Western blot (right) shows interaction on chromatin of the indicated proteins. Input is shown on the left. m Schematic representation for p27/STAT3/cJun in activator (left) and repressor (right) complexes. All graphs show mean ± SEM from N = 3 biological replicate assays. p-values were calculated by paired one-tailed Student’s T Test and are indicated in graphs. Source data are provided as a Source data file.

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