Researchers Identify New Suppressor Effects of the NOX4 Protein in Liver Cancer

Researchers of the TGF-beta and Cancer group of Bellvitge Biomedical Research Institute (IDIBELL), in collaboration with King's College London, have unveiled the role of NADPH oxidase NOX4 as an inhibitor of the epithelial-amoeboid transition, a process that contributes to the migration and invasion of tumor cells. The study was published online on December 12, 2016 in Oncogene. The open-access article is titled “The NADPH Oxidase NOX4 Represses Epithelial to Amoeboid Transition and Efficient Tumour Dissemination.” In previous studies, the researchers suggested that NOX4 acts as a tumor suppressor in the liver, through inhibiting cell proliferation. "In this work, we proved that NOX4 also is an important inhibitor of the invasion and metastasis of liver tumor cells," explains Dr. Isabel Fabregat, leader of the IDIBELL research group. In vitro studies indicate that NOX4 silencing in liver tumor cells induces a migratory movement known as “amoeboid.” The amoeboid movement, related to cell contractility, is regulated by the Rho family of proteins; increased expression of these proteins results in this type of movement, associated with aggressive metastases. In the study in hepatocellular carcinoma patients, it was observed that a significant number of cases present NOX4 deletions; in addition, those patients with a low expression of NOX4 and a high expression of Rho proteins had a much worse prognosis. "This gives to our in vitro study a translational relevance, since it brings forward new prognostic biomarkers for this type of cancer", the IDIBELL researcher comments. NOX4 is regulated at the transcriptional level by the TGF-beta cytokine, which has been studied by the research group for more than 15 years.
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