black tea derivative causes cell death of her2 breast cancer cells including ER+ones

[Lani]

Toxicol Appl Pharmacol. 2006 Nov 10; [Epub ahead of print]
Theanaphthoquinone inhibits fatty acid synthase expression in EGF-stimulated human breast cancer cells via the regulation of EGFR/ErbB-2 signaling.

Weng MS,
Ho CT,
Ho YS,
Lin JK.
Graduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, No. 1, Section 1, Jen-Ai Road, Taipei 10018, Taiwan.
Fatty acid synthase (FAS) is a major lipogenic enzyme catalyzing the synthesis of long-chain saturated fatty acids. Most breast cancers require lipogenesis for growth. Here, we demonstrated the effects of theanaphthoquinone (TNQ), a member of the thearubigins generated by the oxidation of theaflavin (TF-1), on the expression of FAS in human breast cancer cells. TNQ was found to suppress the EGF-induced expression of FAS mRNA and FAS protein in MDA-MB-231 cells. Expression of FAS has previously been shown to be regulated by the SREBP family of transcription factors. In this study, we demonstrated that the EGF-induced nuclear translocation of SREBP-1 was blocked by TNQ. Moreover, TNQ also modulated EGF-induced ERK1/2 and Akt phosphorylation. Treatment of MDA-MB-231 cells with PI 3-kinase inhibitors, LY294002 and Wortmannin, inhibited the EGF-induced expression of FAS and nuclear translocation of SREBP-1. Treatment with TNQ inhibited EGF-induced EGFR/ErbB-2 phosphorylation and dimerization. Furthermore, treatment with kinase inhibitors of EGFR and ErbB-2 suggested that EGFR/ErbB-2 activation was involved in EGF-induced FAS expression. In constitutive FAS expression, TNQ inhibited FAS expression and Akt autophosphorylation in BT-474 cells. The PI 3-kinase inhibitors and tyrosine kinase inhibitors of EGFR and ErbB-2 also reduced constitutive FAS expression. In addition, pharmacological blockade of FAS by TNQ decreased cell viability and induced cell death in BT-474 cells. In summary, our findings suggest that TNQ modulates FAS expression by the regulation of EGFR/ErbB-2 pathways and induces cell death in breast cancer cells.

[RhondaH]

a couple of cups of black tea a day (in addition to my 4 cups of green). Take care and God bless.

Rhonda

[RhondaH]

this was in Consumer Reports 11/05. Take care and God bless.

Rhonda

Black tea may be as good as green

"Good news for tea drinkers: Black tea, the type consumed by most North Americans, appears to pack roughly the same amount of disease-fighting antioxidants as green tea, despite green’s reputation as the healthier brew. Both teas are made from the same plant, but black is oxidized, which darkens the leaves, before it’s processed. When Consumer Reports last measured the two teas’ ability to neutralize damaging molecules called free radicals--a standard test of antioxidant power--green and black teas scored comparably high. While it’s not clear whether the body absorbs the antioxidants from black tea as readily as those from green, observational studies of tea drinkers suggest comparable reductions in the risk of disease for both brews. Presumably the same is true for oolong tea, which is oxidized less than black tea."

[Lani]

that tested a compound against her2+ breast cancer lines, including one that was ER+ even.

Most articles just say xxxxx is good or bad against breast cancer--but as we all know breast cancers are as different as apples are from oranges, bananas, plums and pineapples.

Now that you are all hungry...
Merry Christmas!