LSD1 facilitates erythroid lineage-linked metabolic phenotype. RNA-sequencing analysis. Venn diagrams of genes upregulated (A) and downregulated (B) more than 1.2-fold by LSD1-KD and S2101 treatment (10 µM) are indicated (left). Gene ontology (GO) analysis of the gene sets significantly upregulated and downregulated by LSD1 inhibition (right). Top 10 pathways with statistical significance are indicated with log₁₀P values. Pathways related to heme synthesis (upregulated) and membrane-bound proteins (downregulated) are highlighted in red and blue, respectively. (C) Schema of hemoglobin synthesis pathway (left). qRT-PCR data showing expression changes of hemoglobin biosynthesis genes in LSD1-KD HEL cells (right). (D) Light microscopy image of benzidine-stained HEL cells (left). Arrows represent benzidine-positive cells. Proportions of benzidine-positive cells (right). The experiment was triplicated by calculating 1000 cells in each assay. (E) Metabolomic analysis of LSD1-inhibited HEL cells. Cells were treated with hemin and S2101 and were subjected to capillary electrophoresis time of flight mass spectrometry–based metabolomic analysis. (F-G) Expression changes of non-erythroid hematopoietic markers in LSD1-KD– and S2101-treated HEL cells. All histogram data are mean ± standard deviation of triplicate results. *P < .05, **P < .01 vs control. ALA, 5′-aminolevulinic acid; CPgen III, coproporphyrinogen III; PP IX, protoporphyrin IX.