What is it about?
In this report, we first demonstrated that 9-cis-RA induced CBR3 expression in an OSCC cell line, Ca9-22. The induced expression of the CBR3 protein in Ca9-22 cells caused suppression of proliferation and cell motility. Furthermore, the CBR3 mRNA expression was markedly reduced in OSCCs compared to that in pre-malignant dysplasias and hyperplasias. Among OSCCs, the expression of CBR3 was significantly down-regulated in highly invasive tumors compared with less invasive ones.
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Why is it important?
Our results suggesting that CBR3 is a mediator of cytostatic effects by RA in OSCC cells.
Perspectives
CBR was originally identified as a cytosolic NADPH-dependent oxido-reductase that reduced a wide variety of carbonyl compounds. It has been isolated from a number of human tissues including brain, liver, breast, ovary and placenta. Its actions are identical to prostaglandin 9-ketoreductase that inactivates prostaglandin E2 (PGE2) by converting to PGF2a, which is a potent stimulator of vascular endothelial growth factor (VEGF). Further analysis of the function and regulatory mechanism of the CBR3 gene should clarify its roles in oral malignancy.
Dr Nobuo Kondoh
Asahi University
Read the Original
This page is a summary of: Carbonyl Reductase 3 (CBR3) Mediates 9-cis-Retinoic Acid-Induced Cytostatis and is a Potential Prognostic Marker for Oral Malignancy, The Open Dentistry Journal, June 2008, Bentham Science Publishers,
DOI: 10.2174/1874210600802010078.
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