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It explains seven major oncoviruses that manipulate metabolic pathways and GLUT expression, especially GLUT1, to support viral replication and oncogenesis. 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BMC Cancer (2024) 24:1329 BMC Cancer  \n[https://doi.org/10.1186/s12885-024-13013-y](https://doi.org/10.1186/s12885-024-13013-y)  \nREVIEW Open Access  \nA narrative review: exploring viralinduced malignancies through the lens of dysregulated cellular metabolism and glucose transporters  \nAmirhossein Shahpar 1, Vahideh Hamidi Sofiani2, Nazanin Zeinali Nezhad3, Marzieh Charostad4, Reza Ghaderi 1, Niloofar Farsiu 1, Amin Karimzadeh Kiskani5, Sara Pezeshki6 and Mohsen Nakhaie 1,5*  \nAbstract  \nIntroduction In this narrative review, we unravel the complex interplay between oncogenic viruses, cellular metabolism, and glucose transporter (GLUT) dysregulation in viral-induced malignancies.  \nMethods By explaining the diverse mechanisms through which seven major oncoviruses manipulate metabolic pathways and GLUT expression, particularly GLUT1, we provide novel insights into the critical role of metabolic reprogramming in viral replication and oncogenesis.  \nResults Our exploration of the molecular pathways targeted by viral oncoproteins reveals a similarity between the metabolic alterations induced by viral infections and those observed in neoplastic transformation. A key finding of our review is the overexpression of GLUTs, particularly GLUT1, as a hallmark of both viral infections and many cancers. Conclusions By elucidating the complex interplay between viral oncoproteins, oncogene activation, tumor suppressor gene loss, and GLUT overexpression, we highlight the potential of GLUTs as novel targets for diagnosis, prognosis, and therapy of viral-induced malignancies.  \nKeywords Glucose transporters (GLUTs), Metabolic reprogramming, Viral infections, Cancer metabolism, Warburg effect  \n*Correspondence:  \nMohsen Nakhaie  \n[mohsennakhaee1367@gmail.com](mohsennakhaee1367@gmail.com)  \n1Gastroenterology and Hepatology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran  \n2Department of Microbiology, Golestan University of Medical Sciences, Gorgan, Iran  \n3Physiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran  \n4Department of Biology, Faculty of Science, Yazd University, Yazd, Iran 5Clinical Research Development Unit, Afzal ipour Hospital, Kerman University of Medical Sciences, Kerman, Iran  \n6Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran  \n© The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit [http://](http://)[ ](http://)[creativecommons.org/l](creativecommons.org/l)icenses/by-nc-nd/4.0/.  \nShahpar et al. BMC Cancer (2024) 24:1329 Page 2 of 15  \nBackground  \nThe recent update of the “Hallmarks of Cancer” review has underscored the significance of metabolic transformation in cancer cells, identifying dysregulation of cellular metabolism as an emerging hallmark. This altered metabolism is a critical player in oncogenesis, driven by the activation of oncogenes and the loss of tumo","cbCaikGxaQDTq3B0","https://ap.wps.com/l/cbCaikGxaQDTq3B0","pdf",2409633,15,"English","# Introduction\n## Interplay between oncogenic viruses, cellular metabolism, and GLUT dysregulation\n# Methods\n## Mechanisms of oncoviruses manipulating metabolic pathways and GLUT expression\n# Results\n## Similarities between viral-induced metabolic alterations and neoplastic transformation\n## GLUT overexpression, especially GLUT1, as a shared hallmark\n# Conclusions\n## GLUTs as targets for diagnosis, prognosis, and therapy","[{\"question\":\"What does the review focus on in viral-induced malignancies?\",\"answer\":\"The review focuses on the interplay between oncogenic viruses, dysregulated cellular metabolism, and abnormal glucose transporter (GLUT) regulation.\"},{\"question\":\"How do oncoviruses influence cellular metabolism and GLUT expression?\",\"answer\":\"By explaining diverse mechanisms used by seven major oncoviruses to manipulate metabolic pathways and GLUT expression, particularly GLUT1.\"},{\"question\":\"Why are GLUTs proposed as targets for diagnosis, prognosis, and therapy?\",\"answer\":\"Because the review links viral oncoprotein activity and oncogenic changes with GLUT overexpression, identifying GLUTs—especially GLUT1—as a hallmark across viral infections and many cancers.\"}]","A narrative review: exploring viral-induced malignancies through the lens of dysregulated cellular metabolism and glucose transporters | PDF",1789999040,38]