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Table 1 Impact of GN-25 treatment on transcription factor programs in Kras-HMLE-SNAIL cells

From: Systems analysis reveals a transcriptional reversal of the mesenchymal phenotype induced by SNAIL-inhibitor GN-25

Transcription factor Expression treated/untreated Predicted activation state Regulation z-score p-value of overlap
TBX2 -2.005 Inhibited -2.978 1.91E-04
MYC -2.245 Inhibited -2.912 1.52E-08
NR3C1 -3.751 Inhibited -2.654 1.21E-08
TWIST1 -4.096 Inhibited -2.028 3.92E-02
GLI1 2.264 Activated 2.073 3.00E-02
SMAD7 2.005 Activated 2.079 4.17E-06
DDIT3 8.076 Activated 2.110 1.06E-02
CEBPA 4.142 Activated 2.189 9.86E-05
HOXA5 3.132 Activated 2.189 1.27E-01
TFEB 2.098 Activated 2.339 3.92E-02
IRF1 3.651 Activated 2.506 2.84E-02
XBP1 2.026 Activated 3.415 4.11E-01
IRF7 3.915 Activated 3.894 1.32E-04
TP53 NS Activated 3.502 4.57E-18
  1. Transcription factors whose expression levels (fold-change, treated versus untreated) and predicted activation state are significantly changed by GN-25 treatment in HMLE-SNAIL cells specifically compared to HMLE cells. Although the expression levels of TP53 was not significantly (NS) changed by GN-25 treatment in HMLE-SNAIL cells, its function was predicted to be inhibited in untreated HMLE-SNAIL cells, but activated by GN-25 treatment. Myc-target genes in the data set significantly overlap with a gene set with clinical outcome (dead at 3 years) (Additional file3: Table S2). GN-target genes in the data set overlap significantly with the 3 year clinical outcome metastatic outcomes. Oncomine query matching VV and Koa, respectively.