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. 2017 Oct 4;36(21):3139–3155. doi: 10.15252/embj.201797994

Figure 3. Key transcriptional memory gene Hoxa9 may help to overcome β‐catenin‐dependent transformation in LSK‐derived MLL‐CSCs.

Figure 3

  • A
    Gene set enrichment analysis (GSEA) shows “Targets of Hoxa9/Meis1, down” (Hess et al, 2006) for the indicated comparison.
  • B
    Log10‐fold FDR q‐values of the indicated gene sets positively enriched in β‐catenin‐deleted LSK‐MLL‐ENL compared to β‐catenin‐deleted GMP‐MLL‐ENL.
  • C–E
    RNA‐seq log2‐fold change of key self‐renewal genes (C), RT–qPCR validation of Hox/Meis1 expression represented as mean ± SD of three independent experiments. Two‐tailed t‐test was performed (D), and GSEA showing “Hoxa9_dn.v1_up” (Faber et al, 2009) for the β‐catenin‐deleted LSK‐MLL‐ENL to β‐catenin‐deleted GMP‐MLL‐ENL comparison (E).
  • F
    Colony numbers in serial replating assay of indicated MLL‐ENL‐transduced cells. Data are represented as mean ± SD (n = 3).
  • G
    Kaplan–Meier survival curve of mice transplanted with Hoxa9 −/− (n = 18) or WT LSK‐MLL‐ENL (n = 13) transformed cells (solid lines) and secondary recipient mice (n = 5 for Hoxa9 −/− and n = 4 for wt, dotted lines) as indicated. Comparisons between Hoxa9 WT and Hoxa9 −/− were not significantly different (ns).
Data information: See also Appendix Fig S3.