['The tumor suppressor genes p15(INK)⁴(b) and p16(INK)⁴(a) as well as the estrogen receptor-α (ESR1) gene are abnormally methylated and expressed in colon cancer. The cancer-preventative abilities of several bioactive food components have been linked to their estrogenic and epigenetic activities.', 'The effect of folic acid, zebularine, resveratrol, genistein and epigallocatechin-3-gallate (EGCG) on tumor cell growth, promoter methylation of ESR1, p15(INK)⁴(b) and p16(INK)⁴(a) and gene expression of ESR1 and ESR2 was analyzed in Caco-2 cells. Gene expression was measured using real-time PCR, and promoter CpG methylation was assessed using bisulfite conversion and methylation-specific PCR.', 'After exposure to a high concentration of folic acid (20 μmol/l), enhanced cancer cell growth and concomitant increased methylation of the ESR1 (3.6-fold), p16(INK)⁴(a) and p15(INK)⁴(b) promoters was observed. A lower concentration of folic acid (2 μmol/l) decreased cell growth. The phytoestrogens genistein and resveratrol enhanced expression of ESR1 (genistein 200 μmol/l: 2.1-fold; resveratrol 50 μmol/l: 6.3-fold) and ESR2 (2.6- and 3.6-fold, respectively). Genistein and resveratrol treatment increased promoter methylation of ESR1 (genistein 200 μmol/l: 2.9-fold; resveratrol 50 μmol/l: 1.4-fold). For p16(INK)⁴(a), increased methylation was found after exposure to 10 μmol/l resveratrol, but for p15(INK)⁴(b), decreased methylation was found. Both components showed growth-inhibitory activities. For EGCG, growth inhibition at 100 μmol/l and suppressed promoter methylation of tumor suppressor genes (p16(INK)⁴(a): 0.9-fold; p15(INK)⁴(b): 0.6-fold) was seen.'] Is epigenetic control of estrogen receptor expression and tumor suppressor genes modulated by bioactive food compounds?