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The effect of trastuzumab alone and combined with α‐linolenic acid, γ‐tocopherol, sesame lignan and its metabolites on the growth of BT‐474 and MCF‐7 human breast cancer cells
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.887.5
Subject(s) - enterolactone , mcf 7 , lignan , medicine , trastuzumab , breast cancer , sesamin , growth inhibition , apoptosis , cancer , pharmacology , endocrinology , cancer research , chemistry , biochemistry , traditional medicine , human breast , phytoestrogens , stereochemistry , estrogen
About 25% of breast cancers overexpress epidermal growth factor receptor‐2 (HER2), are aggressive and mainly treated with trastuzumab (TRAS). Our objective was to determine the effect of some food components on the proliferation of breast cancer cells which overexpress HER2 (BT‐474) and those which have physiological HER2 levels (MCF‐7). Using a 4‐day in‐vitro incubation method, we examined the effect of sesame lignan (sesamin, SES, 1 uM), its metabolites (enterodiol (ED) and enterolactone (EL), 1 uM), α‐linolenic acid (ALA, 50 uM), and γ‐tocopherol (GTOC, 20 uM), alone and combined with TRAS (10 μg/ml). Compared with control, in MCF‐7 cells, tumor reduction was 33% (P<0.001) with ALA alone, 9% (P<0.05) with ALA combined with TRAS, and none with the others. In BT‐474 cells, there were 53% and 35% tumor reductions with TRAS and ALA alone (P<0.001), respectively, 20% tumor increase with GTOC (P<0.01) and no effect with the other treatments. Tumor reductions were observed with TRAS co‐treatment with SES (59%), ED (62%), EL (57%), ALA (61%), and GTOC (64%) (all P<0.001), however they did not differ from TRAS treatment alone in BT‐474 cells. In conclusion, ALA is the most effective anti‐cancer food component in both cell lines. Although other treatments are less effective, they and ALA do not antagonize the effectiveness of TRAS in HER2 overexpressing tumors.