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. Author manuscript; available in PMC: 2022 Jan 6.
Published in final edited form as: Cancer Discov. 2021 Jun 14;11(10):2544–2563. doi: 10.1158/2159-8290.CD-20-0872

Figure 2: Napabucasin is potent and selective against FLC.

Figure 2:

(A) Workflow for generation of PDX and high throughput drug screening. (B) Normalized percent survival of FLC1-6 and PHH treated with napabucasin, additional inhibitors of the EIF4F complex (SBI-0640756 and CR-1-31-B) or Ryuvidine (a SETD8 protein lysine methyltransferase (PKMT) inhibitor). (C) Expression levels of STAT3 by differential expression analysis from RNA-Seq in non-tumor liver (N), tumors (T) and PDX (P). (D) Immunohistochemical staining for pSTAT3 on a section of FLC1, showing positive staining only in the stroma (Scale bar: 50μm). (E) Normalized percent survival of cells from FLC1 treated with the STAT3 inhibitors C188-9 (red) and HO3867 (blue). (F) Differential expression analysis of oxidoreductases (NQO1, CBR1, POR, NFE2L2, TXN in non-tumor liver (N), tumors (T) and PDX (P), from RNA-Seq. (G) Normalized percent survival of cells from FLC1 treated with different drugs in the presence (red) or absence (blue) of N-acetylcysteine (NAC) 10mM. (H,I) Effect of napabucasin (1μM or 2μM) on eIF4F sensitive protein levels of (H) c-myc with GAPDH control and (I) MDM2, Bcl-xL, MCL1, Cyclin D1, C/EBP with GAPDH control, in FLC6 cells.