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CD147 and downstream ADAMTSs promote the tumorigenesis of Kaposi sarcoma-associated herpesvirus

ABSTRACT: The Kaposiâs Sarcoma-associated Herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposiâs Sarcoma (KS), which preferentially arise in immunocompromised patients but lack of effective therapeutic options. We have previously shown that KSHV or viral protein LANA can upregulate the glycoprotein CD147 (Emmprin) to induce primary endothelial cell invasiveness, which also requires PI3K/Akt and MAPK activation of VEGF production. In the current study, we first time identify the global network controlled by CD147 in KSHV-infected endothelial cells using Illumina microarray analysis. Among these downstream genes, ADAMTS1 and 9, two specific metalloproteases are strongly expressed in AIDS-KS tissues and contributed to KSHV-infected cell invasiveness through regulation of related cytokines production and respective receptors expression. By using a nude mice KS-like model, we found that targeting CD147 and downstream ADAMTSs proteins significantly suppressed KSHV-related tumorigenesis in vivo, which is potentially through impairing extracellular matrix (ECM) formation in tumor microenvironment. Taken together, we think that targeting CD147 and related proteins may represent a promising therapeutic strategy against KSHV-related malignancies. HUVEC cells were infected by KSHV or transduced by a CD147 recombinant adenoviral vector and the gene expression signature was compared to respective controls

ORGANISM(S): Homo sapiens

SUBMITTER: Zhiqiang Qin

PROVIDER: E-GEOD-69067 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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CD147 and downstream ADAMTSs promote the tumorigenesis of Kaposi sarcoma-associated herpesvirus

Project description:The Kaposi’s Sarcoma-associated Herpesvirus (KSHV) is the etiologic agent of several human cancers, including Kaposi’s Sarcoma (KS), which preferentially arise in immunocompromised patients but lack of effective therapeutic options. We have previously shown that KSHV or viral protein LANA can upregulate the glycoprotein CD147 (Emmprin) to induce primary endothelial cell invasiveness, which also requires PI3K/Akt and MAPK activation of VEGF production. In the current study, we first time identify the global network controlled by CD147 in KSHV-infected endothelial cells using Illumina microarray analysis. Among these downstream genes, ADAMTS1 and 9, two specific metalloproteases are strongly expressed in AIDS-KS tissues and contributed to KSHV-infected cell invasiveness through regulation of related cytokines production and respective receptors expression. By using a nude mice KS-like model, we found that targeting CD147 and downstream ADAMTSs proteins significantly suppressed KSHV-related tumorigenesis in vivo, which is potentially through impairing extracellular matrix (ECM) formation in tumor microenvironment. Taken together, we think that targeting CD147 and related proteins may represent a promising therapeutic strategy against KSHV-related malignancies.

2016-05-31 | GSE69067 | GEO

Unveiling the Role of KSHV-Infected Human Mesenchymal Stem Cells in Kaposi's Sarcoma Initiation

Project description: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 pro-angiogenic environmental conditions, KSHV can reprogram hMSCs to exhibit gene expression profiles more similar to KS tumors, activating cell cycle progression, cytokine signaling pathways, and endothelial differentiation 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 pro-angiogenic environment.

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The profile of cellular and KSHV microRNAs in AIDS_KS biopsies (and normal skin control biopsies)

Project description:Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognisable by its distinctive red skin lesions. The lesions are KSHV-infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. Here we study the microRNA profiles of the KS lesion biopsies in AIDS patients (including both the cellular and KSHV microRNA). There are (n=3) normal skin biopsies from healthy patients and (n=5) AIDS-KS biopsies. Three of the AIDS-KS biopsies were technically replicated and 2 were single hybridisations.

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Altered global gene profile in KSHV-infected primary oral fibroblasts

Project description:The Kaposi sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi sarcoma (KS), the most common HIV/AIDS-associated tumor worldwide. Involvement of the oral cavity portends a poor prognosis for patients with KS, but mechanisms for KSHV regulation of the oral tumor microenvironment are largely unknown. Infiltrating fibroblasts are found with KS lesions, and KSHV establishes latent infection within human primary fibroblasts in vitro, but contributions for KSHV-infected fibroblasts to the KS microenvironment have not been previously characterized. In the present study, we used Illumina microarray to detect the global gene profile altered in KSHV-infected primary human fibroblasts (PDLF and HGF) isolated from the oral cavity.

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Gene expression profiling of KSHV-infected periodontal ligament cells

Project description:We reported the potential and mechnism of oral mesenchymal stem cell to become Kaposi Sarcoma progenitor cell. Human periodontal ligament cells were infected for 48 hours and 96 hours, then subjected to RNA extraction and sequencing. We found that KSHV-infected PDLSC shared a better similarity with KS biosies in cytokine production, including chemotaxis, angiogenesis, inflammation and differentiation. Furthermore, infection of PDLSC upregulated a spectum of genes involving mesenchymal-to-endothelial differentiation, a process which has been revealed in KS spindle cells. This study reveals the potential and mechnism in which oral mesenchymal stem cell is transformed by KSHV to KS progenitor cell.

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mECK36: a cell and animal model of virally induced Kaposi's sarcoma

Project description:Transfection of a Kaposi's sarcoma (KS) herpesvirus (KSHV) Bacterial Artificial Chromosome (KSHVBac36) into mouse bone marrow endothelial lineage cells generated a cell (mECK36) that induced KS-like tumors in mice. mECK36 formed KSHV-harboring vascularized spindle-cell sarcomas that were LANA+ and displayed a KSHV and host transcriptomes reminiscent of KS tumors. Keywords: Cell type comparison

2007-01-01 | GSE6482 | GEO

Transcription profiling of mouse mECK36: a cell and animal model of virally induced Kaposis sarcoma

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Project description:Kaposi’s Sarcoma (KS) is a heterogenous, multifocal vascular malignancy caused by the human herpesvirus 8 (HHV8), also known as Kaposi’s Sarcoma-Associated Herpesvirus (KSHV). Here, we show that KS lesions express iNOS/NOS2 broadly throughout KS lesions, with enrichment in LANA positive spindle cells. The iNOS byproduct 3-nitrotyrosine is also enriched in LANA positive tumor cells and colocalizes with a fraction of LANA-nuclear bodies. We show that iNOS is highly expressed in the L1T3 tumor model of KS. iNOS expression correlated with KSHV lytic cycle gene expression, which was elevated in late-stage tumors (>4 weeks) but to a lesser degree in early stage (1 week) xenografts. Further, we show that L1T3 tumor growth is sensitive to an inhibitor of nitric oxide, L-NMMA. These finding suggest that iNOS is expressed in KSHV infected endothelial-transformed tumor cells in KS, that iNOS expression depends on tumor microenvironment stress conditions, and that iNOS enzymatic activity contributes to KS tumor growth.

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The profile of cellular and KSHV microRNAs in AIDS_KS biopsies (and normal skin control biopsies)

2009-09-30 | GSE16353 | GEO

PDGFRA Defines the Mesenchymal Stem Cell Kaposi’s Sarcoma Progenitors by Enabling KSHV Oncogenesis in an Angiogenic Environment [ChIP-seq]

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