Mientrung Institute for Scientific Research, Vietnam Academy of Science and Technology (VAST), 321 Huynh Thuc Khang, Hue city, Thua Thien Hue 531600, Vietnam.
Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon, Gangwon-Do 200-701, Republic of Korea.
Biomed Res Int. 2018 Dec 16;2018:3120972. doi: 10.1155/2018/3120972. eCollection 2018.
Degalactotigonin () and three other steroidal compounds solasodine (), -acetyl solasodine (), and soladulcoside A () were isolated from the methanolic extract of , and their chemical structures were elucidated by spectroscopic analyses. The isolated compounds were evaluated for cytotoxic activity against human pancreatic cancer cell lines (PANC1 and MIA-PaCa2) and lung cancer cell lines (A549, NCI-H1975, and NCI-H1299). Only degalactotigonin () showed potent cytotoxicity against these cancer cell lines. Compound induced apoptosis in PANC1 and A549 cells. Further study on its mechanism of action in PANC1 cells demonstrated that significantly inhibited EGF-induced proliferation and migration in a concentration-dependent manner. Treatment of PANC1 cells with degalactotigonin induced cell cycle arrest at G0/G1 phase. Compound induced downregulation of cyclin D1 and upregulation of p21 in a time- and concentration-dependent manner and inhibited EGF-induced phosphorylation of EGFR, as well as activation of EGFR downstream signaling molecules such as Akt and ERK.
从 中甲醇提取物中分离得到达格尔酸酮苷()和另外三种甾体化合物茄啶()、-乙酰茄啶()和索拉杜考苷 A(),并通过光谱分析阐明了它们的化学结构。对分离得到的化合物进行了人胰腺癌细胞系(PANC1 和 MIA-PaCa2)和肺癌细胞系(A549、NCI-H1975 和 NCI-H1299)的细胞毒性活性评价。只有达格尔酸酮苷()对这些癌细胞系表现出很强的细胞毒性。化合物在 PANC1 和 A549 细胞中诱导细胞凋亡。对其在 PANC1 细胞中的作用机制的进一步研究表明,达格尔酸酮苷以浓度依赖的方式显著抑制 EGF 诱导的增殖和迁移。用达格尔酸酮苷处理 PANC1 细胞可诱导细胞周期停滞在 G0/G1 期。该化合物可时间和浓度依赖性地下调 cyclin D1 并上调 p21,并抑制 EGF 诱导的 EGFR 磷酸化以及 EGFR 下游信号分子如 Akt 和 ERK 的激活。