Our newest research article identifies VRK1, a human kinase with chromatin remodelling activity best known for its regulation of cell division and DNA damage response, as a tumor progression marker in neuroblastoma.
VRK1 is an “old friend” from the lab. Previous research (notably the work coming from the laboratory of Prof. Pedro A. Lazo at the Cancer Research Institute in Salamanca) had established VRK1 as a regulator of cell proliferation in other solid tumors, although its role in human physiology goes probably further, considering its links to neurodegenerative disorders and other pathologies. This is the first report delineating VRK1 function in a pediatric tumor like neuroblastoma. We describe VRK1 kinase as an essential gene in neuroblastoma tumor cells, controlling proliferation. VRK1 is associated with tumor aggressiveness and patient survival in Neuroblastoma. Interestingly, we found that VRK1 expression alone is able to stratify patients with agressive disease and worse outcome, even among groups of patients that are now dificcult to classify according to current prognostic markers. This opens up the posibility of using VRK1 expression in the clinical setting in the future.
We have also explored the relationship between VRK1 and the oncogene MYCN, the best-known marker for neuroblastoma progression to date. Our work suggests that VRK1 synergize with MYCN to drive neuroblastoma progression and that VRK1 inhibition may constitute a novel cell-cycle-targeted strategy for anticancer therapy in neuroblastoma. VRK1 specific inhibitors are under development, and they would bring exciting opportunities for the treatment of neuroblastoma and other solid tumors.
Cancer Cell Biology Laboratory 