Sensitization of Human Ovarian Cancer CoC1 Cells to TRAIL-induced Apoptosis by Apigenin
Tang Ai
Abstract
Tang Ai
Abstract
Objective To investigate whether apigenin(API) sensitizes human ovarian cancer CoC1 cells to apoptosis induced by recombinant human soluble TNF-related apoptosis-inducing ligand(TRAIL).Methods Human ovarian cancer CoC1 cells were cultured in vitro.The percentage of sub-G1 cell population was determined by flow cytometry using PI fluorescence staining.Caspase-3 activity was determined using ELISA assay.Results Flow cytometry(FCM) analysis after PI stainning indicated that the percentage of sub-G1 cell population in human ovarian cancer CoC1 cells by API(20μmol/L) or TRAIL(20ng/mL) or both for 48h were 8.83%±2.33%,8.32%±2.80% and 69.50%±4.65%,respectively.Caspase-3 activity in CoC1 cells treated with 20 μmol/L API or 20ng/mL TRAIL or both for 48h was 1.3,1.4,6.5 fold in comparison with medium group.Conclusion API at subtoxic concentration sensitizes induction of apoptosis by TRAIL in human ovarian cancer CoC1 cell line.
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Objective To investigate whether apigenin(API) sensitizes human ovarian cancer CoC1 cells to apoptosis induced by recombinant human soluble TNF-related apoptosis-inducing ligand(TRAIL).Methods Human ovarian cancer CoC1 cells were cultured in vitro.The percentage of sub-G1 cell population was determined by flow cytometry using PI fluorescence staining.Caspase-3 activity was determined using ELISA assay.Results Flow cytometry(FCM) analysis after PI stainning indicated that the percentage of sub-G1 cell population in human ovarian cancer CoC1 cells by API(20μmol/L) or TRAIL(20ng/mL) or both for 48h were 8.83%±2.33%,8.32%±2.80% and 69.50%±4.65%,respectively.Caspase-3 activity in CoC1 cells treated with 20 μmol/L API or 20ng/mL TRAIL or both for 48h was 1.3,1.4,6.5 fold in comparison with medium group.Conclusion API at subtoxic concentration sensitizes induction of apoptosis by TRAIL in human ovarian cancer CoC1 cell line.
Key concepts: Apoptosis, Flow cytometry, Ovarian cancer, Population, Molecular biology, Apigenin, Andrology, Biology