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一篇叙述性综述:通过失调的细胞代谢和葡萄糖转运蛋白的视角探索病毒诱导的恶性肿瘤。

A narrative review: exploring viral-induced malignancies through the lens of dysregulated cellular metabolism and glucose transporters.

机构信息

Gastroenterology and Hepatology Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran.

Department of Microbiology, Golestan University of Medical Sciences, Gorgan, Iran.

出版信息

BMC Cancer. 2024 Oct 29;24(1):1329. doi: 10.1186/s12885-024-13013-y.

Abstract

INTRODUCTION

In this narrative review, we unravel the complex interplay between oncogenic viruses, cellular metabolism, and glucose transporter (GLUT) dysregulation in viral-induced malignancies.

METHODS

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.

RESULTS

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.

摘要

简介

在这篇叙述性评论中,我们揭示了致癌病毒、细胞代谢和葡萄糖转运蛋白(GLUT)失调在病毒诱导的恶性肿瘤中的复杂相互作用。

方法

通过解释七种主要致癌病毒操纵代谢途径和 GLUT 表达(特别是 GLUT1)的不同机制,我们提供了关于代谢重编程在病毒复制和致癌中的关键作用的新见解。

结果

我们对病毒癌蛋白靶向的分子途径的探索揭示了病毒感染引起的代谢改变与肿瘤转化中观察到的改变之间的相似性。我们的综述的一个重要发现是 GLUTs 的过度表达,特别是 GLUT1,是病毒感染和许多癌症的标志。

结论

通过阐明病毒癌蛋白、癌基因激活、肿瘤抑制基因丢失和 GLUT 过度表达之间的复杂相互作用,我们强调了 GLUTs 作为诊断、预后和治疗病毒诱导的恶性肿瘤的新靶标的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4f92/11520837/54b9900847d9/12885_2024_13013_Fig1_HTML.jpg

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