Biological and Pharmaceutical Bulletin · 2008 · 30 citations · 21 references
Life SciencesOncologyPharmacologyApoptosisCancer PharmacologyCell SignalingApoptosis In CancerApoptosis RegulationApoptotic SignalingCancer Cell SignalingColorectal CancerMalignant NeoplasmsAnti-proliferative SignalingAnticancer ActivityCancer Cell Proliferation InhibitionCell ConfluenceCell Growth RegulationMitogen-activated Protein Kinase SignalingWestern Blot AnalysisWestern Blotting
We compared anti-proliferative activities of (-)-epigallocatechin gallate (EGCG) and (-)-epigallocatechin (EGC) against HCT116 colorectal carcinoma cells. These catechins inhibited cell growth to nearly the same extent at low cell confluency in plates. However, their inhibitory effect grew weaker as cell confluence increased, and this tendency was more conspicuous for EGC than for EGCG. Both EGCG and EGC activated the phosphorylation of the major MAPKs, ERK, JNK, and p38, in the HCT116 cells as in many other established human cancer cells though to different extents. Cell cycle analyses, DNA fragmentation assays, and TUNEL assays as well as Western blot assays suggested that these catechins inhibited cell growth through mitogen-activated protein kinase (MAPK)-mediated apoptosis rather than cell cycle regulation.
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Absorption, distribution, elimination of tea polyphenols in rats.
Laishun Chen, Mao‐Jung Lee, He Li et al. · PubMed · 1997 · 460 citations