Khan Muhammad, Rasul Azhar, Yi Fei, Zhong Lili, Ma Tonghui
Central Research Laboratory, Jilin University, Changchun, China.
Asian Pac J Cancer Prev. 2011;12(12):3235-8.
Flavonoid compounds have been shown to trigger cell cycle arrest at G0/G1, S and G2/M checkpoints, allowing cells to repair DNA damage before entry into mitosis. Jaceosidin, a flavonoid compound, has been reported to induce apoptosis in various cancer cell lines. In our previous study, we established that jaceosidin induces apoptosis in U87 glioblastoma cells through G2/M phase arrest. However the molecular mechanisms oremained unclear. In the present study, mRNA and protein expression levels of major cell cycle regulatory genes were analyzed by semi-quantitative RT-PCR and Western blot studies respectively. The results demonstrated that jaceosidin-induced G2/M phase arrest in U87 cells is associated with DNA fragmentation, up-regulation of p53 and p21 and subsequent down-regulation of cyclin B1 and CDK1 expression at mRNA as well as at protein level. These findings provide insights into jaceosidin-induced G2/M phase arrest in U87 glioblastoma cells.
黄酮类化合物已被证明可在G0/G1、S和G2/M检查点触发细胞周期停滞，使细胞在进入有丝分裂之前修复DNA损伤。黄酮类化合物紫铆素已被报道可在多种癌细胞系中诱导细胞凋亡。在我们之前的研究中，我们证实紫铆素通过G2/M期停滞诱导U87胶质母细胞瘤细胞凋亡。然而，其分子机制仍不清楚。在本研究中，分别通过半定量RT-PCR和蛋白质印迹研究分析了主要细胞周期调节基因的mRNA和蛋白质表达水平。结果表明，紫铆素诱导U87细胞G2/M期停滞与DNA片段化、p53和p21上调以及随后细胞周期蛋白B1和CDK1在mRNA和蛋白质水平的表达下调有关。这些发现为紫铆素诱导U87胶质母细胞瘤细胞G2/M期停滞提供了见解。
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