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FEBS Lett. 2010 Jan 4;584(1):7-14. doi: 10.1016/j.febslet.2009.10.081.

Theaflavins retard human breast cancer cell migration by inhibiting NF-kappaB via p53-ROS cross-talk.

Author information

1
Division of Molecular Medicine, Bose Institute, P1/12 CIT Scheme VIIM, Kolkata, India.

Abstract

The present study demonstrates that theaflavins exploit p53 to impede metastasis in human breast cancer cells. Our data suggest that p53-dependent reactive oxygen species (ROS) induce p53-phosphorylation via p38MAPK in a feedback loop to inhibit IkappaBalpha-phosphorylation and NF-kappaB/p65 nuclear translocation, thereby down-regulating the metastatic proteins metalloproteinase (MMP)-2 and MMP-9. When wild-type p53-expressing MCF-7 cells are transfected with p53 short-interfering RNA, or treated with a pharmacological inhibitor of ROS, theaflavins fail to inhibit NF-kappaB-mediated cell migration. On the other hand, NF-kappaB over-expression bestows MCF-7 cells with resistance to the anti-migratory effect of theaflavins. These results indicate that inhibition of NF-kappaB via p53-ROS crosstalk is a pre-requisite for theaflavins to accomplish the anti-migratory effect in breast cancer cells.

PMID:
19883646
DOI:
10.1016/j.febslet.2009.10.081
[Indexed for MEDLINE]
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