Sarcophyton和Sinularia属（Alcyoniidae）的软体珊瑚以卡斯班和棕榈二萜类二萜化合物被广泛认知，且具有显著的抗肿瘤效果。从红海软珊瑚Sinularia leptoclados和Sarcophyton glaucum的有机萃取物中，分离出两种卡斯班型二萜化合物（1、2）和四种棕榈二萜型二萜化合物（3-6），它们都可以抑制Huh-7、SNU 499和HepG2三种肝细胞癌细胞，以及EA.hy 926正常细胞的增殖。其中Sinueracabanone D（1）对这些癌细胞株具有显著的抗增殖作用，特别是对HepG2细胞具有IC50为4.0±0.37 μM的抑制效果。细胞周期分析显示，化合物1可导致HepG2细胞在G2/M期积累。此外，化合物1表现出显著的促细胞凋亡作用，可通过annexin V染色、增强Bax、细胞色素C和caspase 3的mRNA表达，并抑制Bcl2的表达，从而表明它在HepG2细胞中产生显著的促细胞凋亡效应。同时，化合物1的加入可以增强活性氧分子的产生并降低线粒体膜电位。总之，化合物1具有强大的抗HepG2细胞增殖作用，这些抗增殖作用是通过诱导细胞凋亡、线粒体功能障碍和氧化应激等方式实现的。©2023 Springer Nature，作者独家授权Springer-Verlag GmbH Germany发布。

The soft-bodied corals of the genera Sarcophyton and Sinularia (Alcyoniidae) are known as a warehouse of casbane and cembranoid diterpenoids with remarkable antitumor effects. Two casbane-type diterpenoids (1, 2) along with four cembrane-type diterpenoids (3-6) were isolated from the diethyl ether soluble fraction of the organic extracts of the Red Sea soft corals Sinularia leptoclados and Sarcophyton glaucum, respectively. The antiproliferative activity of all isolated compounds (1-6) against three hepatocellular carcinoma cells, namely, Huh-7, SNU 499, and HepG2, along with the normal cells EA.hy 926, was evaluated. Sinueracabanone D (1) displayed a remarkable antiproliferative effect against the examined cancer cell lines, especially HepG2 cells with IC50 of 4.0 ± 0.37 µM. Cell cycle analysis indicated compound 1 caused the accumulation of HepG2 cells in the G2/M-phase. Further, compound 1 exhibited significant pro-apoptotic activities in HepG2 cells as evidenced by annexin V staining, enhanced mRNA expression of Bax, cytochrome C, and caspase 3, as well as inhibition of Bcl2 expression. Also, challenging HepG2 cells with sinueracabanone D (1) enhanced the active oxygen species generation and decreased mitochondrial membrane potential. In conclusion, compound 1 possesses potent antiproliferative activities against HepG2 cells. These antiproliferative activities are mediated, at least partly, by their ability to induce apoptosis, mitochondrial dysfunction, and oxidative stress.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.