The rise of viperin: the emerging role of viperin in cancer progression
Alyssa G. Weinstein, Inês Godet, Daniele M. Gilkes
Abstract
Metabolic reprogramming is a hallmark of malignancy that allows cancer cells to utilize nutrients and energy to continuously proliferate (1). Proliferating cancer cells have increased rates of glycolysis and macromolecule biosynthesis. While normal cells require extracellular signals to proliferate, cancer cells have metabolic autonomy and do not always need extracellular signals to trigger proliferation (2). The most well-understood metabolic changes that occur during cancer progression include alterations in the PI3K/AKT/mTOR pathway, stabilization of HIF-1, and enhanced expression of MYC genes (3-5). Recent data support the role of IFNs in regulating cancer metabolism; for example, IFNs can activate the JAK/STAT signaling pathway in cancer cells to regulate metabolic processes and activate a tumor immune response (6). However, the role of IFN-stimulated genes (ISGs) in metabolic reprogramming is not fully understood. In this issue of the JCI, Choi, Kim, and co-authors addressed this knowledge gap by examining the role of the IFN-inducible protein viperin in metabolic reprogramming Their data suggest that viperin is the ISG that controls cancer cell metabolism, whereas other ISGs that are upregulated in cancer cells may not alter metabolism.