In the present study, we demonstrate that, in HT-29 human colon carcinoma cells, luteolin 1) reduces IGF-II secretion; 2) inhibits the growth-stimulatory effects of IGF-I; 3) reduces the levels of IGF-IR transcripts and the IGF-IR precursor protein; 4) reduces the IGF-I-induced tyrosine phosphorylation of IGF-IRβ and the association of p85 with IGF-IRβ; 5) inhibits IGF-I-induced PI3K activity 6) inhibits IGF-I-induced Akt activation; and 7) inhibits the IGF-I-induced phosphorylation of ERK1/2 and CDC25c. This evidence concerns the gene IGF1R and colon carcinoma.