4.6 Article

BDE-47 and BDE-209 inhibit proliferation of Neuro-2a cells via inducing GI-phase arrest

Journal

ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 50, Issue -, Pages 76-82

Publisher

ELSEVIER
DOI: 10.1016/j.etap.2016.12.009

Keywords

2,2 '-,4,4 '-tetrabromodiphenyl ether (BDE-47); Decabrominateddiphenyl ether (BDE-209); Neuro-2a cells; Cell proliferation; Cell cycle; G1-phase arrest

Funding

  1. National Natural Science Foundation of China [41476109, 41276140]
  2. National Science Foundation of China [NSFC-U 1406403]
  3. Shandong Province [NSFC-U 1406403]

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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 BDE209 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 cyclinDl 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. (C) 2016 Published by Elsevier B.V.

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