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. 2012 Jun 16;61(12):2321–2331. doi: 10.1007/s00262-012-1301-x

Table 1.

PMA triggers transcriptional increase in NF-κB gene targets in adherent HL-60 cells

Gene name Gene ID Induction by PMA (x-fold) Functional grouping
IL1RN 3557 556 Cytokines/chemokines
CCL5 6352 352 Differentiation, cytokines/chemokines
IL1B 3553 200 Inflammation, cytokines/chemokines
ICAM1 3383 176 Immune response
MMP9 4318 137 Differentiation, apoptosis
IL1A 3552 102 Inflammation, cytokines/chemokines
IL2RA 3559 71 Inflammation
INS 3630 40 Inflammation, apoptosis
CD40 958 27 Immune response
IL8 3576 24 Cytokines/chemokines
F3 2152 23 Anti-apoptosis
PDGFB 5155 22 Stress response
TNSF10 8743 20 Cytokines/chemokines
CD83 9308 15 Immune response
CCL2 6347 14 Immune response, cytokines/chemokines
MITF 4286 12 Differentiation, apoptosis
BIRC3 330 11 Apoptosis
COX2 5743 10 Inflammation, apoptosis
TNFRSF1B 7133 9.7 Apoptosis

Serum-starved HL-60 cells were treated with 3 nM PMA for 18 h. Total RNA was isolated from vehicle-treated cells that remained in suspension and from PMA-treated cells that adhered to the flasks (macrophage-differentiated cells). The identity of only those genes that were induced by tenfold in adherent versus suspension cells is shown and is extracted from Fig. 2a. Data are representative from two independent arrays. Italicized data were further confirmed at the protein and/or activity level