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绞股蓝皂苷可诱导人口腔癌HSC-3细胞死亡并改变其基因表达。

Gypenosides induce cell death and alter gene expression in human oral cancer HSC-3 cells.

作者信息

Lu Kung-Wen, Ma Yi-Shih, Yu Fu-Shun, Huang Yi-Ping, Chu Yung-Lin, Wu Rick Sai-Chuen, Liao Ching-Lung, Chueh Fu-Shin, Chung Jing-Gung

机构信息

College of Chinese Medicine, School of Post-Baccalaureate Chinese Medicine, China Medical University, Taichung 40402, Taiwan, R.O.C.

School of Chinese Medicine for Post-Baccalaureate, I-Shou University, Kaohsiung 84001, Taiwan, R.O.C.

出版信息

Exp Ther Med. 2017 Sep;14(3):2469-2476. doi: 10.3892/etm.2017.4840. Epub 2017 Jul 25.

DOI:10.3892/etm.2017.4840
PMID:28962182
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5609268/
Abstract

Gypenosides (Gyp), the primary components of Makino, have long been used as a Chinese herbal medicine. In the present study, the effects of Gyp on cell viability, the cell cycle, cell apoptosis, DNA damage and chromatin condensation were investigated using human oral cancer HSC-3 cells. The results of the present study indicated that Gyp induces cell death, G2/M phase arrest and apoptosis in HSC-3 cells in a dose-dependent manner. It was also demonstrated that Gyp decreased the depolarization of mitochondrial membrane potential in a time-dependent manner. A cDNA microarray assay was performed and the results indicated that a number of genes were upregulated following Gyp treatment. The greatest increase was a 75.42-fold increase in the expression of GTP binding protein in skeletal muscle. Levels of the following proteins were also increased by Gyp: Serpine peptidase inhibitor, clade E, member 1 by 20.25-fold; ras homolog family member B by 18.04-fold, kelch repeat and BTB domain containing 8 by 15.22-fold; interleukin 11 by 14.96-fold; activating transcription factor 3 by 14.49-fold; cytochrome P450, family 1 by 14.44-fold; ADP-ribosylation factor-like 14 by 13.88-fold; transfer RNA selenocysteine 2 by 13.23-fold; and syntaxin 11 by 13.08-fold. However, the following genes were downregulated by GYP: Six-transmembrane epithelial antigen of prostate family member 4, 14.19-fold; γ-aminobutyric acid A receptor by 14.58-fold; transcriptional-regulating factor 1 by 14.69-fold; serpin peptidase inhibitor, clade B, member 13 by 14.71-fold; apolipoprotein L 1 by 14.85-fold; follistatin by 15.22-fold; uncharacterized LOC100506718; fibronectin leucine rich transmembrane protein 2 by 15.61-fold; microRNA 205 by 16.38-fold; neuregulin 1 by 19.69-fold; and G protein-coupled receptor 110 by 22.05-fold. These changes in gene expression illustrate the effects of Gyp at the genetic level and identify potential targets for oral cancer therapy.

摘要

绞股蓝总皂苷（Gyp）是绞股蓝的主要成分，长期以来一直被用作中药材。在本研究中，使用人口腔癌HSC-3细胞研究了Gyp对细胞活力、细胞周期、细胞凋亡、DNA损伤和染色质凝聚的影响。本研究结果表明，Gyp以剂量依赖性方式诱导HSC-3细胞死亡、G2/M期阻滞和凋亡。还证明Gyp以时间依赖性方式降低线粒体膜电位的去极化。进行了cDNA微阵列分析，结果表明Gyp处理后许多基因上调。最大的增加是骨骼肌中GTP结合蛋白表达增加75.42倍。Gyp还增加了以下蛋白质的水平：丝氨酸蛋白酶抑制剂E家族成员1增加20.25倍；Ras同源家族成员B增加18.04倍，含kelch重复和BTB结构域的8增加15.22倍；白细胞介素11增加14.96倍；激活转录因子3增加14.49倍；细胞色素P450 1家族增加14.44倍；ADP-核糖基化因子样14增加13.88倍；硒代半胱氨酸转运RNA 2增加13.23倍；Syntaxin 11增加13.08倍。然而，以下基因被GYP下调：前列腺家族成员4的六跨膜上皮抗原，下调14.19倍；γ-氨基丁酸A受体下调14.58倍；转录调节因子1下调14.69倍；丝氨酸蛋白酶抑制剂B家族成员13下调14.71倍；载脂蛋白L 1下调14.85倍；卵泡抑素下调15.22倍；未鉴定的LOC100506718；富含亮氨酸的纤连蛋白跨膜蛋白2下调15.61倍；微小RNA 205下调16.38倍；神经调节蛋白1下调19.69倍；G蛋白偶联受体110下调22.05倍。这些基因表达的变化说明了Gyp在基因水平上的作用，并确定了口腔癌治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/538adf44e77d/etm-14-03-2469-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/b6514e06ab20/etm-14-03-2469-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/231c0a14d110/etm-14-03-2469-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/cea50e358f61/etm-14-03-2469-g02.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/540dd1ed6870/etm-14-03-2469-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/5e08233125f3/etm-14-03-2469-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/826ffad741cb/etm-14-03-2469-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/538adf44e77d/etm-14-03-2469-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/b6514e06ab20/etm-14-03-2469-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/231c0a14d110/etm-14-03-2469-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/cea50e358f61/etm-14-03-2469-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/d03bd721f9e3/etm-14-03-2469-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/540dd1ed6870/etm-14-03-2469-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/5e08233125f3/etm-14-03-2469-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/826ffad741cb/etm-14-03-2469-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a64/5609268/538adf44e77d/etm-14-03-2469-g07.jpg

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