Nitric oxide (NO) is a multifunctional regulator, critical to various biochemical processes, including
inflammation, vasodilatation, intra- and intercellular signaling, apoptosis, and
carcinogenesis. In particular, recent studies have indicated the association between elevated NO production and
neoplastic cell transformation, suggesting procarcinogenic effects of NO. To investigate the mechanism by which NO facilitates oral
carcinogenesis, we tested the effects of exogenous NO on the expression of
hnRNP G, a novel
protein demonstrating
tumor suppressive effects against
oral squamous cell carcinomas. Oral epithelial cells exposed to NO donor demonstrated significant reduction in the level of
hnRNP G protein and
mRNA expression. Also, exposure to NO donor led to decreased
hnRNP G promoter activity in cells, indicating that NO negatively regulates
hnRNP G expression at the level of transcription. Since
hnRNP G expression is markedly decreased or completely abolished in precancerous and malignant oral lesions in situ, these results suggest the possibility that NO facilitates the progression of the disease by targeting
hnRNP G expression. In this article, we review the role of
hnRNP G in
tumor suppression and maintenance of genetic integrity, with focus on its potential association with NO in the context of oral
carcinogenesis.