Abstract
Tumor metabolism has been the object of several studies in the past, leading to the pivotal observation of a consistent shift toward aerobic glycolysis (so-called Warburg effect). More recently, several additional investigations proved that tumor metabolism is profoundly affected during tumorigenesis, including glucose, lipid and amino-acid metabolism. It is noticeable that metabolic reprogramming can represent a suitable therapeutic target in many cancer types. Epstein–Barr virus (EBV) was the first virus linked with cancer in humans when Burkitt lymphoma (BL) was described. Besides other well-known effects, it was recently demonstrated that EBV can induce significant modification in cell metabolism, which may lead or contribute to neoplastic transformation of human cells. Similarly, virus-induced tumorigenesis is characterized by relevant metabolic abnormalities directly induced by the oncoviruses. In this article, the authors critically review the most recent literature concerning EBV-induced metabolism alterations in lymphomas.
Highlights
Oncogenic viruses are an important public health issue since they are responsible for 20% of total human cancer cases
Epstein–Barr virus (EBV), is associated with many tumors including nasopharyngeal carcinoma (NPC) and different lymphoma subtypes (Table 1; Luo and Ou, 2015). These oncogenic viruses exert their oncogenic power by interfering with multiple molecular signaling pathways. Sometimes they directly integrate their DNA in the host cell one [as does HPV in cervical cancer cells (Fang et al, 2014) or HBV in hepatocytes inducing hepatocellular carcinoma (HCC) development (Herrmann et al, 1995)], some others they alter the expression of miRNAs (Ambrosio et al, 2014b), and in other cases, they directly interact with proteins expressed by normal or cancer cells
These findings suggest that NF-kB signaling, increasing the glucose import, supports proliferation and resistance of cancer cells (Sommermann et al, 2011) and that EBV has an important role in its activation (Gewurz et al, 2011)
Summary
Oncogenic viruses are an important public health issue since they are responsible for 20% of total human cancer cases. Epstein–Barr virus (EBV), is associated with many tumors including nasopharyngeal carcinoma (NPC) and different lymphoma subtypes (Table 1; Luo and Ou, 2015). These oncogenic viruses exert their oncogenic power by interfering with multiple molecular signaling pathways. Sometimes they directly integrate their DNA in the host cell one [as does HPV in cervical cancer cells (Fang et al, 2014) or HBV in hepatocytes inducing HCC development (Herrmann et al, 1995)], some others they alter the expression of miRNAs (Ambrosio et al, 2014b), and in other cases, they directly interact with proteins expressed by normal or cancer cells (this is the most important pathogenetic way by which HCV induces HCC; Tsai and Chung, 2010)
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