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

Table 2.

EGCG reverses PMA-mediated IκB degradation in adherent HL-60 cells

Gene name Gene ID EGCG inhibition (%) Functional grouping
MMP9 4318 99 Differentiation, apoptosis
CCR5 1234 98 Inflammation
IL1RN 3557 97 Cytokines/chemokines
CD40 958 96 Immune response
VCAM1 7412 96 Differentiation
CXCL1 2919 96 Cytokines/chemokines
CCL5 6352 95 Cytokines/chemokines, development
FASLG 356 95 Apoptosis
IL1B 3553 95 Inflammation, cytokines/chemokines,
COX2 5743 95 Inflammation, apoptosis
CXCL2 2920 94 Cytokines/chemokines
IL1R2 7850 94 Immune response
TNF 7124 94 Inflammation, development, stress response
CXCL10 3627 94 Inflammation
MITF 4286 93 Differentiation, apoptosis
PDGFB 5155 92 Stress response
IL2RA 3559 91 Inflammation
CCL2 6347 90 Immune response, cytokines/chemokines
CXCL9 4283 90 Inflammation

Serum-starved HL-60 cells were treated with either 30 μM EGCG or a combination of 3 nM PMA and 30 μM EGCG for 18 h. Total RNA was isolated from EGCG-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 which expression was inhibited by 90 % and more is shown and is extracted from Fig. 2b. Data are representative from two independent arrays. Italized data were further confirmed at the protein and/or activity level