| Literature DB >> 28135652 |
Hongmei Chen1, Xuexi Tang1, Bin Zhou1, Ningning Xu1, Zhongyuan Zhou1, Kuan Fang1, You Wang2.
Abstract
Cell proliferation is closely related to cell cycle which is strictly regulated by genes and regulatory proteins. In the present study, we comparatively analyzed the toxic effects of BDE-47 and BDE-209 on cell proliferation of Neuro-2a cells, and the possible mechanism was discussed. The results indicated that BDE-47 significantly inhibited the cell proliferation and the cell cycle were arrest at G1 phase, while BDE-209 had little effects on either cell proliferation or cell cycle. qRT-PCR and Western blot assay presented that BDE-47 up-regulated the gene expressions of p53 and p21, which down-regulated the expresseion of cyclinD1 and CDK2, and inhibited retinoblastoma protein (pRb) phosphorylation. This process could effectively arrest the cell cycle at G1 phase, which finally caused the inhibition on Neuro-2a cell proliferation. However, BDE-209 was only up-regulated the gene expressions of p53, also suggested to be involved in the inhibition on Neuro-2a cell proliferation.Entities:
Keywords: 2,2′ -,4,4′-tetrabromodiphenyl ether (BDE-47); Cell cycle; Cell proliferation; Decabrominateddiphenyl ether (BDE-209); G1-phase arrest; Neuro-2a cells
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Year: 2016 PMID： 28135652 DOI： 10.1016/j.etap.2016.12.009
Source DB: PubMed Journal: Environ Toxicol Pharmacol ISSN： 1382-6689 Impact factor: 4.860