Open AccessAlendronate‐anchored PEGylation of ceria nanoparticles promotes human hepatoma cell proliferation via AKT/ERK signaling pathways
Author(s) -
Cheng Heng,
Liao ZhongLi,
Ning LinHong,
Chen HongYan,
Wei ShanShan,
Yang XiaoChao,
Guo Hong
Publication year - 2017
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.949
Subject(s) - protein kinase b , pegylation , apoptosis , mapk/erk pathway , cell growth , polyethylene glycol , cancer research , biocompatibility , cancer cell , chemistry , peg ratio , cancer , signal transduction , pharmacology , cell , medicine , biochemistry , organic chemistry , finance , economics
Previous work has suggested that ceria nanoparticles ( CNP s) have regenerative antioxidant properties, which have motivated researchers to consider CNP s as therapeutic agents for treating a number of diseases, including cancer. Recent studies have shown CNP s to be toxic to cancer cells, to inhibit invasion and sensitize cancer cells to radiotherapy. In addition, several hydrophilic polymers have been used to coat the CNP surface in order to enhance its properties of extensive biocompatibility and systemic nontoxicity to normal cells and tissues. However, the results of previous studies were based on high CNP doses (10 μ g/mL or more), and these doses may cause serious side effects in clinical applications. The impact of low CNP doses on tumor cells remains unknown. In this study, we report experiments indicating that CNP s‐ AL ‐ polyethylene glycol ( PEG )600, a type of surface‐modified CNP that is more stable and less toxic than traditional CNP s could promote proliferation of hepatoma cells in a dose‐dependent manner. In addition, further research showed that a low dose (0.01 μ g/mL) of CNP s‐ AL ‐ PEG 600 could reduce hepatoma cell apoptosis and activate AKT / ERK signaling pathways. These results may provide information that is important for using CNP s‐ AL ‐ PEG 600 as a therapeutic agent in clinical cancer treatments.