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Anticancer effect of retinoic acid via AP-1 activity repression is mediated by retinoic acid receptor alpha and beta in gastric cancer cells

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Anticancer effect of retinoic acid via AP-1 activity repression is mediated by retinoic acid receptor alpha and beta in gastric cancer cells.htm (413bytes)
Date
2002
Author
Wu, Q
吴乔
Chen, ZM
Su, WJ
苏文金
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  • 生命科学-已发表论文 [5876]
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Abstract
To uncover the mechanism,, relating to the anticancer effect of retinoic acids in gastric cancer cells, the mediation of activator protein-1 (AP-1) activity repression by retinoic acid receptors (RARs) was investigated. All-trans retinoic acid (ATRA) inhibited AP-1 activity in BGC-823 cells(RARalpha(+), RARbeta(+)), but not in MKN-45 cells (RARalpha(lo). RARbeta). Transient transfection of RARbeta expression vector into MKN-45 cells significantly resulted in direct repression of AP-1 activity in a receptor concentration-dependent manner, and this could be strengthened by ATRA, Stable transfection of RARbeta into MKN-45 cells directly inhibited cell growth and colony formation, and ATRA also. enhanced these effects. Transient transfection of RARalpha into MKN-45 cells however. displayed receptor concentration-dependent AP-1 activity inhibition only in the presence of ATRA. Stable transfection of RARalpha into MKN-45 cells resulted in ATRA-dependent inhibition of cell growth and colony formation. For AP-1 binding activity induced by TPA, the repressive effect of ATRA was only observed in BGC-823 and RARa and RARbeta stably transfected MKN-45 cells, but not in intact MKN-45 cells. This indicates the necessity for sufficient cellular RARa and/or RARbeta in order for AP-1 activity repression to occur. Deletion of DNA binding domain (DBD) of RARbeta, but not ligand binding domain (LBD). eliminated the anti-AP-1 function of RARbeta, It is therefore concluded that both RARalpha and RARbeta are mediators in the anticancer function of ATRA via AP-1 activity inhibition, and that RARbeta, not RARa, can inhibit AP-1 activity to a certain extent directly by itself. Thus DBD, not LBD, is critical for anti-AP-1 activity. (C) 2002 Elsevier Science Ltd. All rights reserved.
Citation
Int J Biochem Cell Biol. 2002 Sep;34(9):1102-14
URI
http://dx.doi.org/doi:10.1016/S1357-2725(02)00030-4
https://dspace.xmu.edu.cn/handle/2288/11058

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