2012年1月22日，據《每日科學》報導，木犀草素，一種常見於水果和蔬菜中的黃酮類化合物。在實驗室條件下，這種化合物被證明具有抗炎、抗氧化和抗癌特性，但來自流行病學研究的結果不那麼確定。發表於BMC Gastroenterology上的一項新研究表明，木犀草素能夠抑制結腸癌細胞中對於癌症生長非常重要的細胞信號通路（IGF和PI3K）。
結腸癌是西方國家第二大常見癌症相關死亡的原因。與正常的結腸組織相比，結腸癌細胞中的IGF-II水平升高。據認為，這是驅動細胞不受控制的分裂及癌症生長的機制的一部分。來自韓國的研究人員發現，木犀草素能夠阻止結腸癌細胞分泌IGF-II並在2小時內降低受體（IGF-IR）前體蛋白的總量。木犀草素也減少了活性受體的總量（通過IGF-I依賴的磷酸化測量）。
木犀草素抑制了IGF-I的生長刺激作用，由Jung Han Yoon Park教授領導的小組發現，木犀草素影響了在癌症中由IGF-I激活的細胞信號通路。Jung Han Yoon Park教授解釋說，木犀草素降低了PI3K、Akt、ERK1/2和CDC25c細胞信號通路中IGF-I依賴的激活。阻斷這些通路能阻止癌細胞的分裂並導致癌細胞死亡。
Jung Park教授繼續說，"我們的研究表明，木犀草素幹擾了結腸癌細胞中的細胞信號，這為了解這種黃酮物質如何作用邁出了一步。更全面的了解體內研究結果對於確定它如何可能被開發成一種有效的化學預防劑至關重要。"（生物谷bioon.com）
Luteolin decreases IGF-II production and downregulates insulin-like growth factor-I receptor signaling in HT-29 human colon cancer cells
Do Young Lim, Han Jin Cho, Jongdai Kim, Chu Won Nho, Ki Won Lee and Jung Han Yoon Park
Abstract (provisional)： Background： Luteolin is a 3',4',5,7-tetrahydroxyflavone found in various fruits and vegetables. We have shown previously that luteolin reduces HT-29 cell growth by inducing apoptosis and cell cycle arrest. The objective of this study was to examine whether luteolin downregulates the insulin-like growth factor-I receptor (IGF-IR) signaling pathway in HT-29 cells. Methods： In order to assess the effects of luteolin and/or IGF-I on the IGF-IR signaling pathway, cells were cultured with or without 60 micromol/L luteolin and/or 10 nmol/L IGF-I. Cell proliferation, DNA synthesis, and IGF-IR mRNA levels were evaluated by a cell viability assay, [3H]thymidine incorporation assays, and real-time polymerase chain reaction, respectively. Western blot analyses, immunoprecipitation, and in vitro kinase assays were conducted to evaluate the secretion of IGF-II, the protein expression and activation of IGF-IR, and the association of the p85 subunit of phophatidylinositol-3 kinase (PI3K) with IGF-IR, the phosphorylation of Akt and extracellular signal-regulated kinase (ERK)1/2, and cell division cycle 25c (CDC25c), and PI3K activity. Results： Luteolin (0 - 60 micromol/L) dose-dependently reduced the IGF-II secretion of HT-29 cells. IGF-I stimulated HT-29 cell growth but did not abrogate luteolin-induced growth inhibition. Luteolin reduced the levels of the IGF-IR precursor protein and IGF-IR transcripts. Luteolin reduced the IGF-I-induced tyrosine phosphorylation of IGF-IR and the association of p85 with IGF-IR. Additionally, luteolin inhibited the activity of PI3K activity as well as the phosphorylation of Akt, ERK1/2, and CDC25c in the presence and absence of IGF-I stimulation. Conclusions： The present results demonstrate that luteolin downregulates the activation of the PI3K/Akt and ERK1/2 pathways via a reduction in IGF-IR signaling in HT-29 cells; this may be one of the mechanisms responsible for the observed luteolin-induced apoptosis and cell cycle arrest.