Studies from Fukui Prefectural University Yield New Data on Breast Cancer [Quercetin-3-O-glucuronide inhibits noradrenaline-promoted invasion of MDA-MB-231 human breast cancer cells by blocking beta(2)-adrenergic signaling]
By a News Reporter-Staff News Editor at Cancer Weekly -- New research on Oncology is the subject of a report. According to news originating from Fukui, Japan, by NewsRx correspondents, research stated, "Endogenous catecholamines such as adrenaline (A) and noradrenaline (NA) are released from the adrenal gland and sympathetic nervous system during exposure to stress. The adrenergic system plays a central role in stress signaling, and excessive stress was found to be associated with increased production of reactive oxygen species (ROS)."
Our news journalists obtained a quote from the research from Fukui Prefectural University, "Overproduction of ROS induces oxidative damage in tissues and causes the development of diseases such as cancer. In this study, we investigated the effects of quercetin-3-O-glucuronide (Q3G), a circulating metabolite of quercetin, which is a type of natural flavonoid, on the catecholamine-induced beta(2)-adrenergic receptor (beta(2)-AR)-mediated response in MDA-MB-231 human breast cancer cells expressing beta(2)-AR. Treatment with A or NA at concentrations above 1 mu M generated significant levels of ROS, and NA treatment induced the gene expression of heme oxygenase-1 (HMOX1), and matrix metalloproteinase-2 (MMP-2) and -9 (MMP9). Inhibitors of p38 MAP kinase (SB203580), cAMP-dependent protein kinase (PKA) (H-89), activator protein-1 (AP-1) transcription factor (SR11302), and NF-kappa B and AP-1 (Tanshinone IIA) decreased MMP2 and MMP9 gene expression. NA also enhanced cAMP induction, RAS activation and phosphorylation of ERK1/2. These results suggested that the cAMP-PKA, MAPK, and ROS-NF-kappa B pathways are involved in beta(2)-AR signaling. Treatment with 0.1 mu M Q3G suppressed ROS generation, CAMP and RAS activation, phosphorylation of ERK1/2 and the expression of HMOX1, MMP2, and MMP9 genes. Furthermore, Q3G (0.1 mu M) suppressed invasion of MDA-MB-231 breast cancer cells and MMP-9 induction, and inhibited the binding of [H-3]-NA to beta(2)-AR."
According to the news editors, the research concluded: "These results suggest that Q3G may function to suppress invasion of breast cancer cells by controlling beta(2)-adrenergic signaling, and may be a dietary chemopreventive factor for stress-related breast cancer."
For more information on this research see: Quercetin-3-O-glucuronide inhibits noradrenaline-promoted invasion of MDA-MB-231 human breast cancer cells by blocking beta(2)-adrenergic signaling. Archives of Biochemistry and Biophysics, 2014;557():18-27. Archives of Biochemistry and Biophysics can be contacted at: Elsevier Science Inc, 360 Park Ave South, New York, NY 10010-1710, USA. (Elsevier - www.elsevier.com; Archives of Biochemistry and Biophysics - www.elsevier.com/wps/product/cws_home/622787)
The news correspondents report that additional information may be obtained from S. Yamazaki, Fukui Prefectural Univ, Dept. of Biosci, Fukui 9101195, Japan. Additional authors for this research include N. Miyoshi, K. Kawabata, M. Yasuda and K. Shimoi (see also Oncology).
Keywords for this news article include: Asia, Fukui, Japan, Kinase, Genetics, Oncology, Sugar Acids, Glucuronates, Glucuronides, Breast Cancer, Women's Health, Glucuronic Acids, Enzymes and Coenzymes
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