Researchers from the Departments of Cell Biology and Medical Physiology at the University of Seville have identified that a high expression of the human protein VRK1 is associated with tumour aggressiveness and low survival among neuroblastoma patients. Aggressive neuroblastoma is one of the most common solid childhood cancers and causes disproportionately high mortality in affected children. Although advances have been made in recent years, the outlook for recovery in children affected by aggressive neuroblastoma remains low and a better understanding of this tumour's biology is needed in order to create new treatments and prognostic tools.
Researchers have characterised the function of VRK1 in neuroblastoma tumour cells and have determined that this protein is essential for tumour cell growth and proliferation. "By studying the expression of this protein in tumours, we were able to identify a priori patients where tumour progression is going to be worse, even in groups where current tools do not predict that behaviour," notes Francisco M. Vega.
This study suggests that VRK1 works in conjunction with other oncogenes such as MYCN, which is heavily affected in this cancer, to boost tumour progression and make it more aggressive. Therefore, the researchers suggest that inhibiting VRK1 could be a new strategy for cancer therapy in neuroblastoma. "VRK1 is a protein kinase. These are some of the best targets for targeted cancer treatment, as we can potentially produce inhibitors in the laboratory that override their activity," explains Professor Vega.
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This study was made possible thanks to funding from the Ministry of Science and the Andalusian Regional Government. In addition, the authors are especially grateful to family members and patients with this type of cancer for their cooperation through the Association of Family and Friends of Patients with Neuroblastoma (NEN).
This study is part of the doctoral thesis of Dr. Ana Colmenero-Repiso and was carried out at the Institute of Biomedicine of Seville (IBiS) by researchers from the Department of Cell Biology and the Department of Medical Physiology of the University of Seville, directed by Dr. Francisco M. Vega and Dr. Ricardo Pardal. In addition, it benefited from the international collaboration of researchers from the German Cancer Centre (DKFZ) in Heidelberg, Germany.
Journal
Cancers