Table 1.
Gene Set Enrichment Analysis (GSEA) of cancer cells treated with GSK343 and UNC1999
| Cell line & Treatment | Hallmark in MSigDB | NES | p value | FDR | # of genes in pathways (ratio) | Reference |
|---|---|---|---|---|---|---|
| HCT116: 10 μM GSK343 for 4 h | CHOLESTEROL_HOMEOSTASIS | 0.55 | 1.000 | 0.994 | 10/73 (14%) | Our previous study (GSE83633) |
| HCT116: 5 μM UNC1999 for 4 h | CHOLESTEROL_HOMEOSTASIS | 1.79 | 0.000 | 0.013 | 17/73 (23%) | |
| UNFOLDED_PROTEIN_RESPONSE | 1.57 | 0.020 | 0.003 | 25/112 (22%) | ||
| HepG2: 10 μM GSK343 for 6 h | CHOLESTEROL_HOMEOSTASIS | 1.86 | 0.004 | 0.022 | 25/73 (34%) | This study (GSE129204) |
| A549: 10 μM GSK343 for 6 h | CHOLESTEROL_HOMEOSTASIS | 2.15 | 0.000 | 0.000 | 26/73 (36%) | |
| MTORC1_SIGNALING | 1.67 | 0.000 | 0.031 | 36/197 (18%) | ||
| HepG2: 10 μM GSK343 for 16 h | CHOLESTEROL_HOMEOSTASIS | 1.89 | 0.000 | 0.001 | 37/73 (51%) | |
| PLC5: 10 μM GSK343 for 16 h | CHOLESTEROL_HOMEOSTASIS | 2.88 | 0.000 | 0.000 | 35/73 (48%) | |
| MTORC1_SIGNALING | 2.63 | 0.000 | 0.000 | 55/197 (28%) | ||
| HYPOXIA | 2.35 | 0.000 | 0.000 | 90/198 (45%) | ||
| ESTROGEN_RESPONSE_EARLY | 1.78 | 0.000 | 0.015 | 67/198 (34%) | ||
| REACTIVE_OXIGEN_SPECIES_PATHWAY | 1.77 | 0.005 | 0.012 | 6/45 (13%) | ||
| ANDROGEN_RESPONSE | 1.76 | 0.007 | 0.012 | 24/101 (24%) | ||
| GLYCOLYSIS | 1.76 | 0.000 | 0.011 | 48/198 (24%) | ||
| HEME_METABOLISM | 1.72 | 0.000 | 0.013 | 82/193 (42%) | ||
| UNFOLDED_PROTEIN_RESPONSE | 1.67 | 0.005 | 0.017 | 24/108 (22%) | ||
| FATTY_ACID_METABOLISM | 1.59 | 0.002 | 0.028 | 38/154 (25%) | ||
| UV_RESPONSE_DN | 1.57 | 0.003 | 0.029 | 47/143 (33%) |
Microarray data from EZH2 inhibitor-treated HepG2, PLC5, A549 and HCT116 cells were analyzed by GSEA against hallmark gene sets. Significant (P < 0.01; FDR < 0.05) hallmark gene sets were shown. Although no hallmark gene sets were enriched in HCT116 cells treated with 10 μM GSK343 for 4 h, the result for “CHOLESTEROL_HOMEOSTASIS” hallmark was still listed in table as a comparison.