Mechanisms and in vitro effects of cepharanthine hydrochloride: Classification analysis of the drug-induced differentiallyexpressed genes of human nasopharyngeal carcinoma cells

10Citations
Citations of this article
11Readers
Mendeley users who have this article in their library.

Abstract

Nasopharyngeal carcinoma (NPC) is the most commonly diagnosed head and neck malignancy and is prevalent worldwide. Previous studies have demonstrated the antitumor properties of cepharanthine hydrochloride (CH) in several human cancer cells. However, the action of CH in NPC cells has yet to be determined. In the present study, we investigated the effects of CH in human NPC cell lines including CNE-1 and CNE-2 on cell growth and apoptosis in vitro. Using MTT and ATP-tumor chemosensitivity assays it was found that CH inhibited cell viability. Additionally, flow cytometric and analysis electron microscopy revealed the inhibition of cell cycle progression and reduction of apoptosis, respectively, in human NPC cell lines including CNE-1 and CNE-2 in vitro. To identify the potential action mechanisms of CH, the cDNA microarray analysis results were confirmed by quantitative PCR analysis using a number of genes, including CDKN1A/P21, NR4A1/TR3 and DAXX. In total, 138 upregulated and 63 downregulated genes in CNE-2 cells were treated with CH. According to their biological function, the genes were classified as: i) cell cycle-related genes; ii) DNA repair-related genes; iii) apoptosis-related genes and iv) nuclear factor-κB (NF-κB) transcription factors signal pathways. The results of the present study showed that CH is a potential therapeutic agent against human NPC, and provide rational explanations and a scientific basis for the study of the development of CH in the treatment of NPC.

Cite

CITATION STYLE

APA

Liu, G., Wu, D., LianG, X., Yue, H., & Cui, Y. (2015). Mechanisms and in vitro effects of cepharanthine hydrochloride: Classification analysis of the drug-induced differentiallyexpressed genes of human nasopharyngeal carcinoma cells. Oncology Reports, 34(4), 2002–2010. https://doi.org/10.3892/or.2015.4193

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free