2003TumoriRequires access

As_2O_3 induced cell cycle arrest and apoptosis in ovarian cancer cell line OVCAR-3 cells

Jingdong Zhang

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Abstract

Objective To study the effect of As_ 2 O_ 3 on the proliferation 、cell cycle and apoptosis in ovarian cancer cell line OVCAR-3 cells. Methods The cell growth was measured by MTT assay and colony-forming test, the cell cycle、apoptosis and bcl-2 protein expression were studied by flow cytometry and cell morphology. Results As_ 2 O_ 3 inhibited OVCAR-3 cell growth in dose-dependent manner at 72 hours and the IC50 was 2 μmol /L. After exposure of OVCAR-3 cells to 0.5-5 μmol /L As_ 2 O_ 3 for seven days, the colony-forming was obviously inhibited, the percent of inhibition was all above 40% ( P 0.01). G_ 2 /M phase arrest and apoptosis were induced by 2? μmol /L and 5 μmol /L As_ 2 O_ 3 at 12 hours. Apoptotic cells increased following the decrease of G_ 2 /M phase cells in dose and time-dependent manner. After treatment with 0.5-5 μmol /L As_ 2 O_ 3 12-72 hours, the mitotic and apoptotic cells increased as determined by cell morphology. The expression of bcl-2 protein was significantly decreased after treatment with 0.5-5?μmol /L As_ 2 O_ 3 . Conclusion As_ 2 O_ 3 inhibited the growth of ovarian cancer cell line OVCAR-3 cells and resulted in both M phase arrest and cell apoptosis.

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Objective To study the effect of As_ 2 O_ 3 on the proliferation 、cell cycle and apoptosis in ovarian cancer cell line OVCAR-3 cells. Methods The cell growth was measured by MTT assay and colony-forming test, the cell cycle、apoptosis and bcl-2 protein expression were studied by flow cytometry and cell morphology. Results As_ 2 O_ 3 inhibited OVCAR-3 cell growth in dose-dependent manner at 72 hours and the IC50 was 2 μmol /L. After exposure of OVCAR-3 cells to 0.5-5 μmol /L As_ 2 O_ 3 for seven days, the colony-forming was obviously inhibited, the percent of inhibition was all above 40% ( P 0.01). G_ 2 /M phase arrest and apoptosis were induced by 2? μmol /L and 5 μmol /L As_ 2 O_ 3 at 12 hours. Apoptotic cells increased following the decrease of G_ 2 /M phase cells in dose and time-dependent manner. After treatment with 0.5-5 μmol /L As_ 2 O_ 3 12-72 hours, the mitotic and apoptotic cells increased as determined by cell morphology. The expression of bcl-2 protein was significantly decreased after treatment with 0.5-5?μmol /L As_ 2 O_ 3 . Conclusion As_ 2 O_ 3 inhibited the growth of ovarian cancer cell line OVCAR-3 cells and resulted in both M phase arrest and cell apoptosis.

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Available abstract

Objective To study the effect of As_ 2 O_ 3 on the proliferation 、cell cycle and apoptosis in ovarian cancer cell line OVCAR-3 cells. Methods The cell growth was measured by MTT assay and colony-forming test, the cell cycle、apoptosis and bcl-2 protein expression were studied by flow cytometry and cell morphology. Results As_ 2 O_ 3 inhibited OVCAR-3 cell growth in dose-dependent manner at 72 hours and the IC50 was 2 μmol /L. After exposure of OVCAR-3 cells to 0.5-5 μmol /L As_ 2 O_ 3 for seven days, the colony-forming was obviously inhibited, the percent of inhibition was all above 40% ( P 0.01). G_ 2 /M phase arrest and apoptosis were induced by 2? μmol /L and 5 μmol /L As_ 2 O_ 3 at 12 hours. Apoptotic cells increased following the decrease of G_ 2 /M phase cells in dose and time-dependent manner. After treatment with 0.5-5 μmol /L As_ 2 O_ 3 12-72 hours, the mitotic and apoptotic cells increased as determined by cell morphology. The expression of bcl-2 protein was significantly decreased after treatment with 0.5-5?μmol /L As_ 2 O_ 3 . Conclusion As_ 2 O_ 3 inhibited the growth of ovarian cancer cell line OVCAR-3 cells and resulted in both M phase arrest and cell apoptosis.

Key concepts: Apoptosis, Cell cycle, Flow cytometry, Cell growth, Cell culture, Cell cycle checkpoint, Mitosis, Molecular biology

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