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. 2024 Mar 6;51(5):63. doi: 10.3892/or.2024.8722

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Copyright: © 2024 Zheng et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 5. — HIF1α is modified by SUMOylation at different lysine sites. (A) Expression of total PIAS4, HIF1α and VHL in Hct116 and LoVo PDCs transfected with siRNA PIAS4-315, 493, 1134, PC, NC and MC, respectively. (B) Expression of cytoplasmic PIAS4, HIF1α and VHL in Hct116 and LoVo PDCs transfected with siRNA PIAS4-315, 493, NC and MC, respectively. (C) The expression of nuclear PIAS4, HIF1α and VHL in Hct116 and LoVo PDCs transfected with siRNA PIAS4-315, 493, NC and MC, respectively. (D) Histograms showing the expression of total, plasma and nuclear PIAS4, HIF1α and VHL in Hct116 and LoVo PDCs and PDCs after PIAS knockdown. (E) The expression of total, cytoplasmic and nuclear HIF1α was detected by western blotting Hct116 and LoVo PDCs before and after transfection with wild type HIF1α, K391R, K477R, K391R and K477R double mutants. ***P<0.001, ****P<0.0001, ns, no significance. PIAS4, protein inhibitor of activated STAT protein 4; HIF1α, Hypoxia inducible factor 1 alpha; VHL, von Hippel-Lindau disease tumor suppressor; si, short interfering; PDCs, daughter cells; PC, positive control; NC, negative control; MC, mock control; PGCCs, polyploid giant cells; Tre, PGCCs with PDCs.