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

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

doi:10.3892/etm.2017.4840

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

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

Affiliations: 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., School of Dentistry, China Medical University, Taichung 40402, Taiwan, R.O.C., Department of Physiology, School of Medicine, China Medical University, Taichung 40402, Taiwan, R.O.C., Department of Food Science, International College, National Pingtung University of Science and Technology, Pingtung 91201, Taiwan, R.O.C., Department of Anesthesiology, China Medical University Hospital, Taichung 40402, Taiwan, R.O.C., Department of Health and Nutrition Biotechnology, Asia University, Taichung 41354, Taiwan, R.O.C., Department of Biological Science and Technology, China Medical University, Taichung 40402, Taiwan, R.O.C.
Published online on: July 25, 2017 https://doi.org/10.3892/etm.2017.4840
Pages: 2469-2476
Copyright: © Lu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Gypenosides (Gyp), the primary components of Gynostemma pentaphyllum 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 in vitro 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.