Abstract
Background EGCG ((−)-epigallocatechin-3-O-gallate), a polyphenol in green tea, induces apoptotic cell death in cancer cells without affecting normal cells and several clinical trials have been carried out to evaluate its potential value [1,2]. 67kDa laminin receptor (67LR) has been identified as an EGCG receptor [3]. It has recently been demonstrated that overexpressed 67LR in multiple myeloma (MM) mediates EGCG-induced cancer-specific apoptosis [4-6]. In this study, we revealed that cGMP acts as a cell death mediator of the EGCG-induced anti-MM effect through acid sphingomyelinase (ASM) activation. In this apoptosis
Highlights
EGCG ((−)-epigallocatechin-3-O-gallate), a polyphenol in green tea, induces apoptotic cell death in cancer cells without affecting normal cells and several clinical trials have been carried out to evaluate its potential value [1,2]. 67kDa laminin receptor (67LR) has been identified as an EGCG receptor [3]
We demonstrated that cGMP negative regulator, phosphodiesterase 5 (PDE5), was overexpressed in MM cells, and vardenafil, PDE5 inhibitor synergically enhanced the anti-MM effect of EGCG
We show the upregulation of cGMP is rate-determining process of this cell death pathway
Summary
EGCG ((−)-epigallocatechin-3-O-gallate), a polyphenol in green tea, induces apoptotic cell death in cancer cells without affecting normal cells and several clinical trials have been carried out to evaluate its potential value [1,2]. 67kDa laminin receptor (67LR) has been identified as an EGCG receptor [3]. It has recently been demonstrated that overexpressed 67LR in multiple myeloma (MM) mediates EGCG-induced cancer-specific apoptosis [4,5,6].
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