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RARα mediates all‐ trans ‐retinoic acid‐induced VEGF‐C, VEGF‐D, and VEGFR3 expression in lung cancer cells
Author(s) -
Kalitin Nikolay N.,
Karamysheva Aida F.
Publication year - 2016
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10587
Subject(s) - retinoic acid , retinoid x receptor , retinoid x receptor alpha , retinoid x receptor gamma , retinoic acid receptor , retinoid x receptor beta , retinoid , retinoic acid receptor alpha , nuclear receptor , cancer research , receptor , vascular endothelial growth factor , chemistry , retinoic acid receptor beta , transcription factor , biology , microbiology and biotechnology , biochemistry , vegf receptors , gene
The regulation of vascular endothelial growth factors C (VEGF‐C) and D (VEGF‐D), and their receptor VEGFR3 gene and protein expression by all‐ trans ‐retinoic acid (atRA) in A549 lung cancer cells, was investigated. We showed that atRA treatment increased VEGF‐C, VEGF‐D, and VEGFR3 protein and mRNA contents in dose‐dependent manner. atRA‐mediated increase of both ligands and receptor expression correlated with the elevated level of retinoic acid receptor α (RARα) expression, while the level of another atRA receptor, peroxisome proliferator‐activated receptor β/δ (PPARβ/δ), was decreased. We demonstrated that the classical counterpart of RARα, retinoid X receptor α (RXRα), was down‐regulated in both cytoplasm and nucleus of A549 cells upon atRA addition. On the contrary, the nuclear quantity of another possible RARα counterpart, transcription factor Sp1, was increased after atRA treatment.