Luteolin is a flavonoid commonly found in fruit and vegetables. This compound has been shown in laboratory conditions to have anti-inflammatory, anti-oxidant and anti-cancer properties but results from epidemiological studies have been less certain. New research published in BioMed Central's open access journal BMC Gastroenterology shows that luteolin is able to inhibit the activity of cell signaling pathways (IGF and PI3K) important for the growth of cancer in colon cancer cells.
Colon cancer is the second most frequent cause of cancer-related death in the Western World. Colon cancer cells have elevated levels of IGF-II compared to normal colon tissues. It is thought that this is part of the mechanism driving uncontrolled cell division and cancer growth. Researchers from Korea showed that luteolin was able to block the secretion of IGF-II by colon cancer cells and within two hours decreased the amount of receptor (IGF-IR) precursor protein. Luteolin also reduced the amount of active receptor (measured by IGF-I dependent phosphorylation).
Luteolin inhibited the growth stimulatory effect of IGF-I and the team led by Prof Jung Han Yoon Park found that luteolin affected cell signaling pathways which are activated by IGF-I in cancer. Prof Jung Han Yoon Park explained, "Luteolin reduced IGF-I-dependent activation of the cell signaling pathways PI3K, Akt, and ERK1/2 and CDC25c. Blocking these pathways stops cancer cells from dividing and leads to cell death."
Prof Jung Park continued, "Our study, showing that luteolin interferes with cell signaling in colon cancer cells, is a step forward in understanding how this flavonoid works. A fuller understanding of the in vivo results is essential to determine how it might be developed into an effective chemopreventive agent."
- Do Young Lim, Han Jin Cho, Jongdai Kim, Chu Won Nho, Ki Won Lee and Jung Han Yoon Park. Luteolin decreases IGF-II production and downregulates insulin-like growth factor-I receptor signaling in HT-29 human colon cancer cells. BMC Gastroenterology, 2012 [link]
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