J Cancer 2018; 9(15):2723-2733. doi:10.7150/jca.26339

Research Paper

Differentially expressed genes of HepG2 cells treated with gecko polypeptide mixture

Yi-Meng Duan, Ying Jin, Meng-Li Guo, Leng-Xin Duan, Jian-Gang Wang

Medical College Department of Pharmacy, Henan University of Science and Technology, Luoyang 471023, Henan Province, China

Abstract

Gecko (Gekko japonicus) extracts have been used in traditional Chinese medicine for many years. It has been proven that the gecko polypeptide mixture (GPM) extracted from gecko can inhibit the growth of multiple types of tumor cells. In order to investigate the possible anti-tumor molecular mechanisms of GPM, we used RNA-seq technology to identify the differentially expressed genes (DEGs) of human hepatocellular carcinoma (HCC) HepG2 cells treated with or without GPM. MTT assay was used to detect the viability of HepG2 cells. DAPI fluorescence staining was performed to observe morphological changes in the nuclei of HepG2 cells. Western blot analysis was applied to observe the expressions of apoptosis-related and endoplasmic reticulum stress (ERS)-related proteins in HepG2 cells. Flow cytometry assay was performed to detect the apoptosis and reactive oxygen species (ROS) in HepG2 cells. Our results showed that GPM inhibited HepG2 cells proliferation and induced the apoptosis of HepG2 cells. RNA-seq analysis suggested that the ER-nucleus signaling pathway involved in the anti-cancer molecular mechanism of GPM. Therefore, GPM may induce apoptosis in HepG2 cells via the ERs pathway.

Keywords: gecko, RNA-seq technology, hepatocellular carcinoma, reactive oxygen species, apoptosis

This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Duan YM, Jin Y, Guo ML, Duan LX, Wang JG. Differentially expressed genes of HepG2 cells treated with gecko polypeptide mixture. J Cancer 2018; 9(15):2723-2733. doi:10.7150/jca.26339. Available from http://www.jcancer.org/v09p2723.htm