| dc.description.abstract | The overall objective of this dissertation was to investigate the effects of green tea catechins (GTCs), especially epigallocatechin-3-gallate (EGCG), on the growth of human placental trophoblasts. The first chapter was to study whether EGCG induced growth inhibition of human placental choriocarcinoma cells. Using BeWo, JEG-3, and JAR choriocarcinoma cells, we discovered that EGCG suppressed the proliferation of all three of the choriocarcinoma cells in dose-dependent and time-dependent manners. A catechin-specific effect of green tea was evident; EGCG was more effective than epicatechin (EC), epicatechin gallate (ECG), and epigallocatechin (EGC) in suppressing cell growth. We found that EGCG suppressed choriocarcinoma cell growth via the AMPK, ERK, and p38 but not JNK pathways. The second chapter was to investigate whether EGCG affects mitogenesis in human villous trophoblasts (HVT). We discovered that EGCG was more effective than other GTCs in suppressing cell growth. Also, the specific inhibitors of ERK1/2, p38, or AMPK blocked EGCG-induced decreases in both cell number and bromodeoxyuridine (BrdU) incorporation, as well as respectively blocking EGCG-stimulated activities of MEK1, p38, and AMPK proteins. Moreover, EGCG was similar to the specific inhibitor of PI3K by inhibiting AKT phosphorylation, cell number and BrdU incorporation. These data imply that EGCG inhibits the growth of HVT through the ERK, p38, AMPK and AKT pathways. We concluded that EGCG acts as an anti-proliferative agent on both normal villous trophoblasts and cancerous trophoblasts can be similar through the ERK, P38, and AMPK pathways, and different through the PI3K/AKT pathways. | en_US |