LSD1 inhibition induces differentiation and cell death in Merkel cell carcinoma

A

Volcano plot showing the −log₁₀ (adjusted P‐value) and log₂ fold change (log₂FC) for transcripts detected by RNAseq analysis of PeTa cells treated with 100 nM GSK‐LSD1 or DMSO for 6 days. Significantly up‐ and downregulated genes (FDR ≤ 0.05; abs[log₂FC] ≥ 1) are marked in red and blue, respectively.

B

Immunoblot analysis for histone marks and LSD1 upon GSK‐LSD1 and protein level quantification normalized to loading control (vinculin) and relative to DMSO control.

C

Pathway enrichment analysis (GO:BP) of 533 significantly downregulated genes upon GSK‐LSD1 treatment displayed in Fig 4D.

D

Pathway enrichment analysis (GO:BP) of 870 significantly upregulated genes upon GSK‐LSD1 treatment displayed in Fig 4F.

E

Cell viability (%) upon 4‐thiouridine (4sU) treatment in PeTa cells over time relative to treatment start (T ₀). Data are represented as means ± SD.

F

Heatmap depicting the transcriptional activation of members of TGFβ signaling after 24‐h treatment with LSD1i.

G

Immunoblot probing for protein levels of phospho‐SMAD1/5/9, ID1, and ID2 in PeTa cells treated with indicated compounds for 24 h. Vinculin serves as loading control.

Figure EV4. LSD1 inhibition induces marked transcriptional changes.