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卡波西肉瘤相关疱疹病毒(KSHV)诱导的癌症及KSHV感染中的代谢重编程与代谢传感器

Metabolic reprogramming and metabolic sensors in KSHV-induced cancers and KSHV infection.

作者信息

Li Tingting, Gao Shou-Jiang

机构信息

Cancer Virology Program, UPMC Hillman Cancer Center, Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, 15213, USA.

出版信息

Cell Biosci. 2021 Sep 27;11(1):176. doi: 10.1186/s13578-021-00688-0.

DOI:10.1186/s13578-021-00688-0
PMID:34579773
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8475840/
Abstract

Kaposi's sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus associated with several human cancers. KSHV infection and KSHV-induced anabolic cell proliferation and cellular transformation depend on reprogramming of cellular metabolic pathways, which provide the building blocks and energy for the growth of both the virus and the infected cells. Furthermore, KSHV dysregulates numerous metabolic sensors including mTOR, AMPK, CASTOR1 and sirtuins to maintain cellular energetic homeostasis during infection and in KSHV-induced cancers. In this review, we summarize the recent advances in the understanding of KSHV hijacking of metabolic pathways and sensors, providing insights into the molecular basis of KSHV infection and KSHV-induced oncogenesis. In addition, we highlight the critical metabolic targets and sensors for developing potential new therapies against KSHV infection and KSHV-induced cancers.

摘要

卡波西肉瘤相关疱疹病毒(KSHV)是一种与多种人类癌症相关的致癌性γ疱疹病毒。KSHV感染以及KSHV诱导的合成代谢细胞增殖和细胞转化依赖于细胞代谢途径的重编程,这些代谢途径为病毒和受感染细胞的生长提供了构建模块和能量。此外,KSHV会失调多种代谢传感器,包括mTOR、AMPK、CASTOR1和sirtuins,以在感染期间以及KSHV诱导的癌症中维持细胞能量稳态。在本综述中,我们总结了对KSHV劫持代谢途径和传感器的理解方面的最新进展,为KSHV感染和KSHV诱导的肿瘤发生的分子基础提供了见解。此外,我们强调了针对开发针对KSHV感染和KSHV诱导的癌症的潜在新疗法的关键代谢靶点和传感器。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/b48f8d2b570c/13578_2021_688_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/5ffb5cd9a863/13578_2021_688_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/f5049a854fb3/13578_2021_688_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/57cac33b0c90/13578_2021_688_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/b48f8d2b570c/13578_2021_688_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/5ffb5cd9a863/13578_2021_688_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/f5049a854fb3/13578_2021_688_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/57cac33b0c90/13578_2021_688_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d18/8477578/b48f8d2b570c/13578_2021_688_Fig4_HTML.jpg

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本文引用的文献

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LKB1 suppresses KSHV reactivation and promotes primary effusion lymphoma progression.LKB1 抑制 KSHV 再激活并促进原发性渗出性淋巴瘤的进展。
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Oncogenic Kaposi's Sarcoma-Associated Herpesvirus Upregulates Argininosuccinate Synthase 1, a Rate-Limiting Enzyme of the Citrulline-Nitric Oxide Cycle, To Activate the STAT3 Pathway and Promote Growth Transformation.致癌性卡波西肉瘤相关疱疹病毒上调精氨琥珀酸合成酶 1,即瓜氨酸-一氧化氮循环的限速酶,以激活 STAT3 通路并促进生长转化。
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