Figure 4.
Hnf4a is a downstream target of TIFAB, negatively regulated by NF-κB. (A) Venn Diagram illustrating genes upregulated or downregulated in TIFAB OE KMT2A::MLLT3 LSPCs (compared with vector-expressed, GSE178853) and Tifab KO LSPCs (compared with WT). Among these genes, 117 were upregulated in TIFAB OE LSPCs while downregulated in Tifab KO LSPCs, including Hnf4a. (B-C) Expression of HNF4A protein in vector- and KMT2A::MLLT3−transduced cKit+ WT BM cells (B) or WT and Tifab KO LSPCs (n = 3). ACTIN served as a loading control. (D-E) Hnf4a mRNA (D) or protein (E) levels in KMT2A::MLLT3 LSPCs expressing either vector, RelA, or RelB. ∗P < .05, Mann-Whitney U test. (F) Higher expression of HNF4A mRNA in patients with AML (TCGA database) correlates with worse survival. P = .0052, log-rank test.

Hnf4a is a downstream target of TIFAB, negatively regulated by NF-κB. (A) Venn Diagram illustrating genes upregulated or downregulated in TIFAB OE KMT2A::MLLT3 LSPCs (compared with vector-expressed, GSE178853) and Tifab KO LSPCs (compared with WT). Among these genes, 117 were upregulated in TIFAB OE LSPCs while downregulated in Tifab KO LSPCs, including Hnf4a. (B-C) Expression of HNF4A protein in vector- and KMT2A::MLLT3−transduced cKit+ WT BM cells (B) or WT and Tifab KO LSPCs (n = 3). ACTIN served as a loading control. (D-E) Hnf4a mRNA (D) or protein (E) levels in KMT2A::MLLT3 LSPCs expressing either vector, RelA, or RelB. ∗P < .05, Mann-Whitney U test. (F) Higher expression of HNF4A mRNA in patients with AML (TCGA database) correlates with worse survival. P = .0052, log-rank test.

Close Modal

or Create an Account

Close Modal
Close Modal