Shi Jun-Yu, Huang Zhe Ren, Gao Hong Yan, Xu Xiao Li
Department of Gynecology, the third Affiliated Hospital of Suzhou University (Changzhou First People's Hospital), Changzhou, Jiangsu Province, China, 213003.
J BUON. 2020 Mar-Apr;25(2):779-784.
Accumulating evidence suggests that Juglone is a potent anticancer molecule of plant origin. However, its anticancer effects have not been fully explored against human ovarian cancer cells. Therefore this study was undertaken to evaluate the anticancer effects of Juglone against the human OVCAR-3 ovarian cancer cells.
Cell viability was evaluated by WST-1 assay. Cellular apoptosis was studied using fluorescence microscopy with DAPI staining. The percentage of OVCAR-3 human ovarian cancer cells was examined by using flow cytometry in combination with annexin V-FITC/propidium iodide (PI) staining. Effects on cell cycle were studied by flow cytometer while effects on cell migration and invasion were evaluated using wound healing and transwell assay, respectively.
Juglone inhibited the growth rate of OVCAR-3 ovarian cancer cells and showed an IC50 of 30 µM. However, Juglone showed very high IC50 (100 µM) against the normal SV40 ovarian cells. DAPI staining showed that Juglone caused nuclear fragmentation of the OVCAR-3 cells, suggestive of apoptosis. Annexin V/PI staining showed that the percentage of the apoptotic OVCAR-3 cells increased from 2.15 in control to 45.24% at 60 µM concentration of Juglone. The induction of apoptosis in the OVCAR-3 cells was also accompanied with activation caspase-3, upregulation of Bax and downregulation of Bcl-2. Juglone was also found to cause an upsurge in the ROS levels in the OVCAR-3 cells. Cell cycle analysis showed that Juglone caused accumulation of the OVCAR-3 cells in the G2/M phase of the cell cycle triggering G2/M cell cycle arrest. Wound healing assay and transwell assay showed that Juglone suppressed the migration as well as the invasion of the OVCAR-3 cells, suggestive of the antimetastatic potential of this molecule.
Juglone may prove advantageous in ovarian cancer treatment.
越来越多的证据表明胡桃醌是一种具有强大抗癌作用的植物源分子。然而，其对人卵巢癌细胞的抗癌作用尚未得到充分研究。因此，本研究旨在评估胡桃醌对人OVCAR-3卵巢癌细胞的抗癌作用。
采用WST-1法评估细胞活力。使用DAPI染色的荧光显微镜研究细胞凋亡。通过流式细胞术结合膜联蛋白V-FITC/碘化丙啶（PI）染色检测OVCAR-3人卵巢癌细胞的百分比。用流式细胞仪研究对细胞周期的影响，同时分别使用伤口愈合试验和Transwell试验评估对细胞迁移和侵袭的影响。
胡桃醌抑制OVCAR-3卵巢癌细胞的生长速率，IC50为30μM。然而，胡桃醌对正常SV40卵巢细胞显示出非常高的IC50（100μM）。DAPI染色显示胡桃醌导致OVCAR-3细胞的核碎片化，提示细胞凋亡。膜联蛋白V/PI染色显示，在60μM浓度的胡桃醌作用下，凋亡的OVCAR-3细胞百分比从对照组的2.15%增加到45.24%。OVCAR-3细胞凋亡的诱导还伴随着半胱天冬酶-3的激活、Bax的上调和Bcl-2的下调。还发现胡桃醌导致OVCAR-3细胞中活性氧水平升高。细胞周期分析表明，胡桃醌导致OVCAR-3细胞在细胞周期的G2/M期积累，引发G2/M期细胞周期阻滞。伤口愈合试验和Transwell试验表明，胡桃醌抑制OVCAR-3细胞的迁移和侵袭，提示该分子具有抗转移潜力。
胡桃醌可能在卵巢癌治疗中具有优势。
