2009
DOI: 10.1016/j.tox.2009.07.023
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CYP1-mediated antiproliferative activity of dietary flavonoids in MDA-MB-468 breast cancer cells

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Cited by 84 publications
(82 citation statements)
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“…39 The anticancer effects of flavonoids occur through oxidative destruction, inhibition of proliferation, inactivation of carcinogen, promotion of differentiation, induction of cell-cycle arrest and apoptosis, impairment of tumor angiogenesis, and suppression of metastasis. [40][41][42] Flavonoids can interact with xenobiotic metabolizing enzymes and inhibit involvement of kinases signal transduction, interact with estrogen type II binding sites, and alter gene expression patterns, 43,44 with resultant promotion of antiproliferative activity of Pd@W.tea NPs.…”
Section: In Vitro Cytotoxicitymentioning
confidence: 99%
“…39 The anticancer effects of flavonoids occur through oxidative destruction, inhibition of proliferation, inactivation of carcinogen, promotion of differentiation, induction of cell-cycle arrest and apoptosis, impairment of tumor angiogenesis, and suppression of metastasis. [40][41][42] Flavonoids can interact with xenobiotic metabolizing enzymes and inhibit involvement of kinases signal transduction, interact with estrogen type II binding sites, and alter gene expression patterns, 43,44 with resultant promotion of antiproliferative activity of Pd@W.tea NPs.…”
Section: In Vitro Cytotoxicitymentioning
confidence: 99%
“…Therapeutic agents include doxorubicin which has known cardiotoxic activity, 38 apigenin which has known cardioprotective activity 39 and luteolin which is a known active metabolite of apigenin. 40 The drug concentration (100 lM) was established from a short incubation (4 h, minimum time to allow for cell adhesion) cytotoxicity curve (data not shown) for apigenin (the least active of the three compounds) in order to identify a concentration that would elicit marginal cell toxicity (IC 25 ) presonication. This concentration was then applied with luteolin and doxorubicin in order to observe whether CA-free sonoporation was achievable for structurally diverse drug molecules, regardless of their initial or intrinsic toxicity.…”
Section: Drug Cytotoxicity Comparison Pre-and Post-sonicationsmentioning
confidence: 99%
“…[17][18][19] It has been postulated that dietary flavonoids exhibit cancer therapeutic effects, due to intracellular CYP1-mediated metabolism to conversion products that inhibit growth of cancerous cells. [16][17][18][19][20] Thus the duality of flavonoids in cancer therapy and prevention is determined by both, their substrate and inhibitor propensities towards CYP1A1 and CYP1B1 enzymes. 16 Inhibition of 7-ethoxyresorufin-O-deethylase activity (EROD) is a well documented assay used predominantly to test the inhibitory potencies of dietary flavonoids.…”
Section: Introductionmentioning
confidence: 99%