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Bioactieve stoffen tegen darmkanker*
De bioactieve stof luteoline en de cafeïnederivaten in mate-thee lijken volgens twee laboratoriumstudies darmkanker te kunnen bestrijden. De eerste studie laat zien hoe luteoline, een bioactieve stof die gevonden wordt in veel groeten en fruit, de aanmaak van bepaalde groeifactoren (IGF en P13K) blokkeert waardoor darmkankerceldeling niet meer plaats kan vinden en de tumor doodgaat. In de tweede studie blijken cafeïnederivaten in mate-thee twee proteïnes (caspase-3 en caspase-8) te activeren waardoor darmkankercellen dood gaan. Deze derivaten in mate bleken ook te zorgen voor duidelijk minder ontstekingsmarkers. De onderzoekers hebben inmiddels ook een studie afgerond met ratten (met darmkanker) die of mate-thee te drinken kregen of gewoon water. De resultaten worden binnenkort gepubliceerd.
Compounds in Mate Tea Induce Death in Colon Cancer Cells, in Vitro Study Shows
Could preventing colon cancer be as simple as developing a taste for yerba mate tea? In a recent University of Illinois study, scientists showed that human colon cancer cells die when they are exposed to the approximate number of bioactive compounds present in one cup of this brew, which has long been consumed in South America for its medicinal properties.
"The caffeine derivatives in mate tea not only induced death in human colon cancer cells, they also reduced important markers of inflammation," said Elvira de Mejia, a U of I associate professor of food chemistry and food toxicology.
That's important because inflammation can trigger the steps of cancer progression, she said.
In the in vitro study, de Mejia and former graduate student Sirima Puangpraphant isolated, purified, and then treated human colon cancer cells with caffeoylquinic acid (CQA) derivatives from mate tea. As the scientists increased the CQA concentration, cancer cells died as a result of apoptosis.
"Put simply, the cancer cell self-destructs because its DNA has been damaged," she said.
The ability to induce apoptosis, or cell death, is a promising tactic for therapeutic interventions in all types of cancer, she said.
de Mejia said they were able to identify the mechanism that led to cell death. Certain CQA derivatives dramatically decreased several markers of inflammation, including NF-kappa-B, which regulates many genes that affect the process through the production of important enzymes. Ultimately cancer cells died with the induction of two specific enzymes, caspase-3 and caspase-8, de Mejia said.
"If we can reduce the activity of NF-kappa-B, the important marker that links inflammation and cancer, we'll be better able to control the transformation of normal cells to cancer cells," she added.
The results of the study strongly suggest that the caffeine derivatives in mate tea have potential as anti-cancer agents and could also be helpful in other diseases associated with inflammation, she said.
But, because the colon and its microflora play a major role in the absorption and metabolism of caffeine-related compounds, the anti-inflammatory and anti-cancer effects of mate tea may be most useful in the colon.
"We believe there's ample evidence to support drinking mate tea for its bioactive benefits, especially if you have reason to be concerned about colon cancer. Mate tea bags are available in health food stores and are increasingly available in large supermarkets," she added.
The scientists have already completed and will soon publish the results of a study that compares the development of colon cancer in rats that drank mate tea as their only source of water with a control group that drank only water.
This in vitro study was published in Molecular Nutrition & Food Research, vol. 55, pp. 1509-1522. Co-authors include Sirima Puangpraphant, now an assistant professor at Kasetsart University in Thailand; Greg Potts, an undergraduate student of the U of I; and Mark A. Berhow and Karl Vermillion of the USDA, ARS, National Center for Agricultural Utilization Research in Peoria, Illinois. The work was funded by the U of I Research Board and Puangpraphant's Royal Thai Government Scholarship.

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 
BMC Gastroenterology 2012, 12:9 doi:10.1186/1471-230X-12-9
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. 
Volledige artikel. (Februari 2012)