Theaflavins retard human breast cancer cell migration by inhibiting NF‐κB via p53‐ROS cross‐talk

Abstract

Edited by Quan Chen Keywords:Breast cancer Migration NF-jB p53 Reactive oxygen species Theaflavins a b s t r a c tThe 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 IjBa-phosphorylation and NF-jB/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-jB-mediated cell migration. On the other hand, NF-jB over-expression bestows MCF-7 cells with resistance to the anti-migratory effect of theaflavins. These results indicate that inhibition of NF-jB via p53-ROS crosstalk is a pre-requisite for theaflavins to accomplish the anti-migratory effect in breast cancer cells. Structured summary:MINT-7295816: p53 (uniprotkb:P04637) physically interacts (MI:0915) with IKK beta (uniprotkb:O14920) by anti bait coimmunoprecipitation (MI:0006)

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Capsaicin-Induced Activation of p53-SMAR1 Auto-Regulatory Loop Down-Regulates VEGF in Non-Small Cell Lung Cancer to Restrain Angiogenesis

“…The data from triplicate wells were calculated as the mean +/− SEM. The migration rate of control cells was taken as 100% and that of other plates were compared with control cells [25].…”

ROS-PIASγ cross talk channelizes ATM signaling from resistance to apoptosis during chemosensitization of resistant tumors

“…For the assessment of cellular ROS, cultured cells or sensitive as well as resistant EAC cells, aseptically drawn within 2 h of drug treatment from the peritoneal cavity of tumor-bearing mice, were incubated for 20 min at 37 °C in the dark with 10  μ M of dichlorofluorescindiacetate (DCFH-DA, Sigma). 48 DCF fluorescence was measured flow cytometrically (Beckton Dickinson FACScan) and subjected to analysis using Cell Quest 3.2 (Beckton Dickinson) software. The probe was excited at 488 nm, and emission was measured through a 530 nm band-pass filter.…”