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揭示卡波西肉瘤起始过程中感染卡波西肉瘤相关疱疹病毒的人间充质干细胞的作用。

Unveiling the role of KSHV-infected human mesenchymal stem cells in Kaposi's sarcoma initiation.

作者信息

Lacunza Ezequiel, Ahuja Anuj, Coso Omar A, Abba Martin, Ramos Juan Carlos, Cesarman Ethel, Mesri Enrique A, Naipauer Julian

机构信息

Centro de Investigaciones Inmunologicas Basicas y Aplicadas, Facultad de Ciencias Medicas, Universidad Nacional de La Plata, La Plata, Argentina.

University of Miami-Centre for AIDS Research/Sylvester Cancer Comprehensive Center Argentina Consortium for Research and Training in Virally Induced AIDS-Malignancies, University of Miami Miller School of Medicine, Miami, Florida, USA.

出版信息

J Med Virol. 2024 May;96(5):e29684. doi: 10.1002/jmv.29684.

DOI:10.1002/jmv.29684
PMID:38773828
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12068558/
Abstract

Kaposi's sarcoma (KS) may derive from Kaposi's sarcoma herpesvirus (KSHV)-infected human mesenchymal stem cells (hMSCs) that migrate to sites characterized by inflammation and angiogenesis, promoting the initiation of KS. By analyzing the RNA sequences of KSHV-infected primary hMSCs, we have identified specific cell subpopulations, mechanisms, and conditions involved in the initial stages of KSHV-induced transformation and reprogramming of hMSCs into KS progenitor cells. Under proangiogenic environmental conditions, KSHV can reprogram hMSCs to exhibit gene expression profiles more similar to KS tumors, activating cell cycle progression, cytokine signaling pathways, endothelial differentiation, and upregulating KSHV oncogenes indicating the involvement of KSHV infection in inducing the mesenchymal-to-endothelial (MEndT) transition of hMSCs. This finding underscores the significance of this condition in facilitating KSHV-induced proliferation and reprogramming of hMSCs towards MEndT and closer to KS gene expression profiles, providing further evidence of these cell subpopulations as precursors of KS cells that thrive in a proangiogenic environment.

摘要

卡波西肉瘤（KS）可能起源于感染卡波西肉瘤疱疹病毒（KSHV）的人间充质干细胞（hMSCs），这些细胞迁移到以炎症和血管生成为特征的部位，促进了KS的起始。通过分析感染KSHV的原代hMSCs的RNA序列，我们确定了KSHV诱导hMSCs转化并重编程为KS祖细胞初始阶段所涉及的特定细胞亚群、机制和条件。在促血管生成的环境条件下，KSHV可将hMSCs重编程，使其表现出更类似于KS肿瘤的基因表达谱，激活细胞周期进程、细胞因子信号通路、内皮分化，并上调KSHV癌基因，表明KSHV感染参与诱导hMSCs的间充质-内皮（MEndT）转变。这一发现强调了这种条件在促进KSHV诱导hMSCs增殖并向MEndT重编程以及更接近KS基因表达谱方面的重要性，进一步证明了这些细胞亚群作为在促血管生成环境中茁壮成长的KS细胞前体的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/88ab5c99792d/nihms-2045162-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/1e826f96ff5d/nihms-2045162-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/e6d47614dafe/nihms-2045162-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/4af0d74e079a/nihms-2045162-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/c9cfbedc56ec/nihms-2045162-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/5c09b57160fc/nihms-2045162-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/0c16276990cd/nihms-2045162-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/88ab5c99792d/nihms-2045162-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/1e826f96ff5d/nihms-2045162-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/e6d47614dafe/nihms-2045162-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/4af0d74e079a/nihms-2045162-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/c9cfbedc56ec/nihms-2045162-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/5c09b57160fc/nihms-2045162-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/0c16276990cd/nihms-2045162-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d09/12068558/88ab5c99792d/nihms-2045162-f0007.jpg

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[1]
Unveiling the role of KSHV-infected human mesenchymal stem cells in Kaposi's sarcoma initiation.

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[5]
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引用本文的文献

[1]
Oncogenic Mechanisms of Kaposi's Sarcoma-Associated Herpesvirus on Cell Metabolism and Cell Transformation.

J Med Virol. 2025-8

[2]
Integrative Functional Genomics Analysis of Kaposi Sarcoma Cohorts.

Res Sq. 2025-3-11

[3]
HIV-1 Tat-induced disruption of epithelial junctions and epithelial-mesenchymal transition of oral and genital epithelial cells lead to increased invasiveness of neoplastic cells and the spread of herpes simplex virus and cytomegalovirus.

Front Immunol. 2025-2-13

本文引用的文献

[1]
The Kaposi's sarcoma progenitor enigma: KSHV-induced MEndT-EndMT axis.

Trends Mol Med. 2023-3

[2]
Kaposi's sarcoma-associated herpesvirus vFLIP promotes MEndT to generate hybrid M/E state for tumorigenesis.

PLoS Pathog. 2021-12

[3]
KSHV enhances mesenchymal stem cell homing and promotes KS-like pathogenesis.

Virology. 2020-10

[4]
Comparative transcriptome analysis of endemic and epidemic Kaposi's sarcoma (KS) lesions and the secondary role of HIV-1 in KS pathogenesis.

PLoS Pathog. 2020-7-24

[5]
PDGFRA defines the mesenchymal stem cell Kaposi's sarcoma progenitors by enabling KSHV oncogenesis in an angiogenic environment.

PLoS Pathog. 2019-12-27

[6]
Kaposi sarcoma.

Nat Rev Dis Primers. 2019-1-31

[7]
RNA-Seq of Kaposi's sarcoma reveals alterations in glucose and lipid metabolism.

PLoS Pathog. 2018-1-19

[8]
Evidence for Kaposi Sarcoma Originating from Mesenchymal Stem Cell through KSHV-induced Mesenchymal-to-Endothelial Transition.

Cancer Res. 2017-10-24

[9]
Human Mesenchymal Stem Cells of Diverse Origins Support Persistent Infection with Kaposi's Sarcoma-Associated Herpesvirus and Manifest Distinct Angiogenic, Invasive, and Transforming Phenotypes.

mBio. 2016-1-26

[10]
Coinfection with human herpesvirus 8 is associated with persistent inflammation and immune activation in virologically suppressed HIV-infected patients.

PLoS One. 2014-8-18

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