Curcumin and Epigallocatechin Gallate Inhibit the Cancer Stem Cell Phenotype via Down-regulation of STAT3–NFκB Signaling

摘要: Background/Aim: The cancer stem cell (CSC) model postulates the existence of a small proportion cells capable sustaining tumor formation, self-renewal and differentiation. Signal Transducer Activator Transcription 3 (STAT3) signaling is known to be selectively activated in breast CSC populations. However, it yet determined which molecular mechanisms regulate STAT3 CSCs what chemopreventive agents are effective for suppressing growth. aim this study was examine potential efficacy curcumin epigallocatechin gallate (EGCG) against uncover their anticancer effects. Materials Methods: To suppress phenotype, two lines (MDA-MB-231 MCF7 transfected with HER2) were treated (10 μM) or without EGCG 48 h. We used tumor-sphere formation wound-healing assays determine phenotype. quantify populations, Fluorescence-activated sorting profiling monitored. phosphorylation interaction Nuclear Factor-kB (NFkB) analyzed by performing western blot immunoprecipitation assays. Results: Combined treatment reduced stem-like Cluster differentiation 44 (CD44)-positive population. Western analyses revealed that specifically inhibited STAT3-NFkB retained. Conclusion: This suggests function as antitumor CSCs. NFκB pathways could serve targets reducing leading novel targeted-therapy treating cancer.