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."
Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central's open access policy.
Article citation and URL available on request at email@example.com on the day of publication.2. BMC Gastroenterology is an open access, peer-reviewed journal that considers articles on all aspects of the prevention, diagnosis and management of gastrointestinal and hepatobiliary disorders, as well as related molecular genetics, pathophysiology, and epidemiology.
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