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. Author manuscript; available in PMC: 2022 Jan 1.
Published in final edited form as: Mol Cancer Res. 2021 Mar 22;19(7):1156–1167. doi: 10.1158/1541-7786.MCR-20-0867

Figure 4. TGM2 as AP-2α target gene and regulator of cell cycle.

Figure 4.

A. ChIP-Seq analysis identified TGM2 as a potential primary target of AP-2α with known AP-2α consensus binding sequences identified at the site of peaks within TGM2 (Supplementary Figure S4). B. Transient knockdown of TGM2 in parental HCT116 with siRNA resulted in a significant increase in the proportion of cells in S/G2/M phase (GFP+) vs. G1 phase (only RFP+) compared to cells treated with siNT, but no change was observed in KO-2 cells (C&D). E. Proposed model suggests TGM2 is a primary target of AP-2α, through which the PI3K/mTOR/AKT pathway is altered, leading to prolongation of S/G2/M phase. F. Data from the GDC Pan-Cancer database demonstrated a correlation between TFAP2A and TGM2 expression. Analysis of a TMA showed no significant difference in TGM2 protein expression comparing AP-2α expressors and non-expressors (G); however, there was a trend in the correlation of TGM2 and AP-2α protein in tumors expressing AP-2α (H).