Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA284440 | ENA |
REPOSITORIES: ENA
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Project description: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
2016-05-31 | E-GEOD-69067 | biostudies-arrayexpress
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
Project description:Assessment of the effect of Kaposi-sarcoma herpesvirus upon the transcriptome of lymphatic endothelial cells and its contribution to the transcriptome of Kaposi sarcoma.
2006-10-23 | E-MEXP-561 | biostudies-arrayexpress
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.
2017-01-01 | GSE79548 | GEO
Project description:Epigenetic consequences of latent infection with Kaposi-sarcoma associated herpesvirus
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Project description:Cancer cells of primary effusion lymphoma (PEL) often contain both Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV). We measured the interplay of human, KSHV, and EBV transcription in a cell culture model of PEL using single-cell RNA sequencing. The data detect widespread trace expression of lytic KSHV genes.
2020-10-13 | GSE154900 | GEO
Project description:The development of a prophylactic vaccine for Kaposi sarcoma-associated Herpesvirus (KSHV) would prevent consequences from infection including disorders such as Kaposi sarcoma and primary effusion lymphoma. Here, we study the immunogenicity of noninfectious virus-like vesicles (VLVs) of KSHV as a potential future vaccine platform. VLVs present a repertoire of viral structural proteins but are noninfectious due to a defect in capsid formation that prevents viral DNA packaging. Immunization of mice with adjuvanted VLVs results in virus-specific antibodies and T cells. These antibodies neutralize viral infection, and this neutralization is enhanced by the complement system. Complement-enhanced neutralization is dependent on antibodies targeting the SCR region of viral ORF4. However, this activity was not present in serum from KSHV-infected humans. Our study highlights an important role of antibody effector functions in the development of a future KSHV vaccine
2023-02-01 | PXD035478 | Pride
Project description:Deregulation of lncRNAs by Kaposi's sarcoma-associated herpesvirus
| PRJNA350313 | ENA