Interestingly, DBCCR1 attenuates the expression of DNMT1 (DNA methyltransferase 1), suggesting a reciprocal regulation between genetic silencing of cancer suppressor genes and activating DNA methylation.
As mice age and NAD<sup>+</sup> concentrations decline, DBC1 is increasingly bound to PARP1, causing DNA damage to accumulate, a process rapidly reversed by restoring the abundance of NAD<sup>+</sup> Thus, NAD<sup>+</sup> directly regulates protein-protein interactions, the modulation of which may protect against cancer, radiation, and aging.
In this review, we will discuss the new developments in DBC1 research, its molecular structure, regulatory roles and implication in metabolism, aging and cancer.
Despite the increasing significance of DBC1 in cancer, the expression of DBC1 and its clinical significance in esophageal squamous cell carcinoma (ESCC) have not been studied.
Our data suggest that hypermethylation of the DBC1 promoter region is a frequent event during the development of lymphoproliferative malignancies, and that DBC1 hypermethylation may serve as a marker for these cancers.