Qian Hao, Huang Tao, Chen Yao, Li Xiucheng, Gong Weihua, Jiang Guangjian, Zhang Wei, Cheng Shuo, Li Xuhui, Li Pengcheng
Department of Orthopedics, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, 02215 MA, USA.
J Cancer Res Ther. 2018 Sep;14(Supplement):S648-S655. doi: 10.4103/0973-1482.203599.
Embelin is an active compound identified as a novel X-linked inhibitor of apoptosis protein (XIAP) inhibitor from the Embelia ribes that exhibits various medicinal effects including anti-inflammatory and anticancer activities. However, the therapeutic effect of Embelin to human osteosarcoma is not yet determined.
In this study, we evaluated the sensitizing potential of Embelin on promoting apoptosis to cause osteosarcoma cell death and inhibiting its invasion.
We uesd 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide to detect the survival rates of osteosarcoma cells, Western blot to detect the expression of proteins in U-2 OS and MG63 cells, and fluorescence microscope to observe the morphology of apoptotic cells.
The survival of osteosarcoma cells decreased, When Embelin was used. Obvious condensed and flared fluorescence was observed, when used high-dose Embelin. There was an increase of caspase-3, cleaved caspase-3, caspase-8, and caspase-9 in Embelin group, while PI3K, AKt, p-AKt, X-linked inhibitor of apoptosis protein, and MMP-9 were downregulated. The invasion of Embelin application was significantly lower than that of the control application.
Embelin promoted apoptosis via XIAP and PI3K/Akt signaling pathway. XIAP inhibitor Embelin inducing apoptosis could cause osteosarcoma cell death and inhibit its invasion.
紫铆因是从紫铆中鉴定出的一种活性化合物，是一种新型的X连锁凋亡蛋白（XIAP）抑制剂，具有多种药用效果，包括抗炎和抗癌活性。然而，紫铆因对人骨肉瘤的治疗效果尚未确定。
在本研究中，我们评估了紫铆因促进凋亡以导致骨肉瘤细胞死亡并抑制其侵袭的致敏潜力。
我们使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐检测骨肉瘤细胞的存活率，蛋白质印迹法检测U-2 OS和MG63细胞中蛋白质的表达，并使用荧光显微镜观察凋亡细胞的形态。
使用紫铆因时，骨肉瘤细胞的存活率降低。使用高剂量紫铆因时，观察到明显的浓缩和扩张荧光。紫铆因组中caspase-3、裂解的caspase-3、caspase-8和caspase-9增加，而PI3K、AKt、p-Akt、X连锁凋亡蛋白抑制剂和MMP-9下调。紫铆因处理组的侵袭明显低于对照处理组。
紫铆因通过XIAP和PI3K/Akt信号通路促进凋亡。XIAP抑制剂紫铆因诱导凋亡可导致骨肉瘤细胞死亡并抑制其侵袭。
