Sasa veitchii extract induces anticancer effects via inhibition of cyclin D1 expression in MCF-7 cells

被引:9
|
作者
Ichimaru, Yoshimi [1 ]
Kanaeda, Natsuki [1 ]
Tominaga, Sarah [1 ]
Suzui, Masumi [2 ]
Maeda, Tohru [1 ]
Fujii, Hirohisa [1 ]
Nakao, Makoto [1 ]
Yoshioka, Hiroki [1 ,3 ]
机构
[1] Kinjo Gakuin Univ, Coll Pharm, Nagoya, Aichi, Japan
[2] Nagoya City Univ, Dept Neurotoxicol, Grad Sch Med Sci, Nagoya, Aichi, Japan
[3] Univ Texas Hlth Sci Ctr Houston, Sch Dent, Ctr Craniofacial Res, 1941 East Rd, Houston, TX 77054 USA
来源
NAGOYA JOURNAL OF MEDICAL SCIENCE | 2020年 / 82卷 / 03期
关键词
Sasa veitchii; cyclin D1; breast cancer; sodium copper chlorophyllin; IN-VITRO; CANCER; CHLOROPHYLLIN; APOPTOSIS; LIGNIN; BAMBOO;
D O I
10.18999/nagjms.82.3.509
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Sasa veitchii and other Sasa species are traditional medicinal herbs belonging to a group of Japanese bamboos collectively called Kumazasa, and these species possess the potential for a wide variety of uses. The present study aimed to elucidate the anticancer mechanisms exerted by S. veitchii extract (SE) against a human breast cancer cell line, MCF-7 cells. Freeze-dried Sunchion (R) was used as the SE, and cell proliferation activity was measured using the [H-3]-thymidine incorporation assay. Induction of apoptosis was accessed via Annexin V and caspase-3 fluorescent staining, the induction of necrosis was measured via pmpidium iodide staining, and cell cycle-related protein expression was determined using western blotting. The IC50 value of the SE was 7.7 mu g/mL in MCF-7 cells. Although the primary active ingredient in Sunchlon (R) is sodium copper chlorophyllin (0.25%), the present results indicated that ingredients other than SCC exert anti-cancer activities (the IC50 value of SCC was 715 mu g/mL), and late apoptosis or necrosis was induced in an SE dose-dependent manner. The expression levels of cyclin D1 and Cdk6 were decreased after SE treatment, and there was no change in the Cdk1/2 expression levels. Additionally, the expression of the necrosis-related cell death indicators RIP1 and RIP3 was increased in response to high-dose SE treatments, and this was indicative of cells preparing for programmed cell death. SE induces cell death in MCF-7 cells via the inhibition of cyclin D1 expression at low concentrations, and this extract induces programmed necrosis (necroptosis) by potentiating RIPURIP3 expression.
引用
收藏
页码:509 / 518
页数:10
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