A B S T R A C TIntroduction To explore the effect of ethynil estradiol and desogestrel onproliferation and apoptosis hydatidiform mole trophoblast cell. Methods: From April2008 until March 2009, we collected 15 samples of hydatidiform mole tissue.Trophoblast cells was isolated and culture at RPMI 20% FBS medium. Only 7samples (46%)shown good growth. Cell was identified using cytology and β HCG test.Trophoblast cells good quality than devided into three groups observation. Firstgroup get ethynil estradiol 10 nmol/mL, second group get desogestrel 100 nmol/mL,Third group get DMSO 1%. Cells incubated and observe at 24, 48, 72, 96 hours. Cellcycle, apoptosis and β HCG was evaluated at each time observation. Cell cycleevaluation using BD cycle test plus DNA reagent, apoptosis evaluation using FITC-Annexin V. Analyze using FACSCalibur flowcytometer. β HCG evaluation usingAbbott AxSym total β-HCG reagent pack. Results: The group of cell that get ethynilestradiol in concentration 10 nmol/mL had cell proliferation index, amount cells andβ HCG level higher than control after 72 hours observation. The group of cell thatget desogestrel in concentration 100 nmol/mL have cell proliferation index, amountcells and β HCG level lower than control after 48 hours observation. There are nodifferences of apoptosis between the two group and control. Conclusion: Ethynilestradiol will increase proliferation of hydatidiform mole trophoblast cell, whiledesogestrel will decrease proliferation of hydatidiform mole trophoblast cell. Thereare no effect of ethynil estradiol and desogestrel on apoptosis of hydatidiform moletrophoblast cell.
Exploration of the regulation and control mechanisms of miR‑145 in trophoblast cell proliferation and invasion
