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Transcription profiling of mouse hemangioendothelioma cell lines EOMA and Py-4-1 models for kaposiform hemangioendotheliomas

ABSTRACT: Kaposiâs sarcoma (KS) is the most frequently occurring malignant tumor in patients infected with the human immunodeficiency virus. Recent studies have revealed that infection of vascular endothelial cells with Kaposi's sarcoma-associated herpes virus in vitro results in a lymphatic re-programming of these cells, with potent induction of the lymphatic marker genes podoplanin and VEGFR-3 which is mediated by upregulation of the transcription factor Prox1. However, the potential effects of Prox1 expression on the biology of KS and, in particular, on the aggressive and invasive behavior of KS tumors in vivo have remained unknown. We stably expressed Prox1 cDNA in the two mouse hemangioendothelioma cell lines EOMA and Py-4-1, well-established murine models for kaposiform hemangioendothelioma. Surprisingly, we found that expression of Prox1 was sufficient to induce a more aggressive behavior of tumors growing in syngenic mice, leading to enhanced local invasion into the muscular layer and to cellular anaplasia. This enhanced malignant phenotype was associated with upregulation of several genes involved in proteolysis, cytoskeletal reorganisation and migration. Together, these results indicate that Prox1 plays an important, previously unanticipated role in mediating the aggressive behavior of vascular neoplasms such as Kaposi's sarcoma. Experiment Overall Design: Total cellular RNA was extracted from two stably Prox1-expressing Py-4-1 cell clones and from two control-transfected Py-4-1 cell clones.

ORGANISM(S): Mus musculus

SUBMITTER: Jay Woo Shin

PROVIDER: E-GEOD-8171 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Prox-1 promotes invasion of kaposiform hemangioendotheliomas

Project description:Kaposi’s sarcoma (KS) is the most frequently occurring malignant tumor in patients infected with the human immunodeficiency virus. Recent studies have revealed that infection of vascular endothelial cells with Kaposi's sarcoma-associated herpes virus in vitro results in a lymphatic re-programming of these cells, with potent induction of the lymphatic marker genes podoplanin and VEGFR-3 which is mediated by upregulation of the transcription factor Prox1. However, the potential effects of Prox1 expression on the biology of KS and, in particular, on the aggressive and invasive behavior of KS tumors in vivo have remained unknown. We stably expressed Prox1 cDNA in the two mouse hemangioendothelioma cell lines EOMA and Py-4-1, well-established murine models for kaposiform hemangioendothelioma. Surprisingly, we found that expression of Prox1 was sufficient to induce a more aggressive behavior of tumors growing in syngenic mice, leading to enhanced local invasion into the muscular layer and to cellular anaplasia. This enhanced malignant phenotype was associated with upregulation of several genes involved in proteolysis, cytoskeletal reorganisation and migration. Together, these results indicate that Prox1 plays an important, previously unanticipated role in mediating the aggressive behavior of vascular neoplasms such as Kaposi's sarcoma. Keywords: Overexpression of Prox1 in Py-4-1 cell line.

2008-08-04 | GSE8171 | GEO

Transcription profiling of mouse mECK36: a cell and animal model of virally induced Kaposis 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. Experiment Overall Design: There are three biological replicates per sample. Tumors (mKS) were compared the the human KS signature. mECK36 and mEC-V were compared to putative BM lineage cells.

2008-06-14 | E-GEOD-6482 | biostudies-arrayexpress

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

2007-01-01 | GSE6482 | 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.

2024-07-08 | GSE260925 | GEO

RNA-binding protein RPS27 and gene expression regulation in human umbilical vein endothelial cells (HUVECs)

Project description:RPS27, a significantly down-regulated and validated RBP in kaposi's sarcoma (KS), and known to be associated with viral infection. As KS is an endothelial cell cancer, we used HUVECs as the cell model to explore the functions of RPS27. RNA-seq technology was used to investigate the differentially expressed genes in HUVECs. By using small interference RNAs (siRNAs) to silence the expression of RPS27 (siRPS27), we detected significant decrease of RPS27 expression in RNA levels comparing with the negative control (siNC) samples.

2024-03-31 | GSE255600 | GEO

Targeting sphingosine kinase by ABC294640 induces KSHV-infected endothelial cell autophagic death

Project description:KSHV is a principal causative agent of Kaposi's Sarcoma (KS). Despite this knowledge about the close relationship between sphingolipid metablism and solid tumors development, the role of sphingolipid metablism in KSHV-related malignancies remains mostly unclear. We report that targeting sphingosine kinase 2 (SphK2) by a selective inhibitor, ABC294640, significantly induces KSHV+ TIVE-LTC autophagic death. By using microarray analysis, we have identified the global gene profile affected by ABC294640 within KSHV+ TIVE-LTC and several novel “druggable” candidates closely related to cancer cell survival/growth. Finally, we found that targeting TIVE-LTC by ABC294640 effectively suppressed KSHV tumorigenicity by using a KS-like nude mice model.

2016-11-01 | GSE74338 | GEO

CD109 is novel KSHV entry receptor in human endothelial cells and enhances infection during cellular senescence

Project description:The aging process is characterized by cellular functional decline and increased susceptibility to infections. Understanding the association between virus infection and aging is crucial for developing effective strategies against viral infections in older individuals. Kaposi's sarcoma-associated herpesvirus (KSHV) infection increases the risk of Kaposi's sarcoma, a vascular cancer prevalent among the elderly without HIV infection. However, the relationship between KSHV pathogenesis and cellular senescence remains unknown. Here, we demonstrate that KSHV infectivity is significantly increased in senescent human endothelial cells due to enhanced binding of virions to cell surface. Proteomic analysis identified caveolin-1 and CD109 that promote KSHV infection and were significantly upregulated in senescent cells. In particular, CD109 is expressed on cell surface and directly interacts with KSHV virions to enhance KSHV infection. Knockout of CD109 abolished while overexpression of CD109 promote KSHV binding to cell surface, and infectivity. These results identify CD109 as a novel KSHV entry receptor that enhances KSHV infection in senescent cells, which might in part explain the higher sensitivity of elder subjects to KSHV infection and Kaposi's sarcoma.

2024-04-17 | PXD048212 | Pride

Genome-wide small RNA sequencing analysis of KSHV long-term-infected endothelial (LTC) and parental uninfected TIVE cells [miRNA-seq]

Project description:Purpose: To characterize genome-wide microRNA (miRNA) expression profiles in the context of Kaposi’s sarcoma-associated herpesvirus (KSHV)-induced oncogenesis using isogenic cell lines for a Kaposi's sarcoma (KS) xenograft model: KSHV-infected human endothelial cells (LTC) that form tumors with properties closely resembling KS lesions in nude mice and uninfected parental (TIVE) cells. Methods: miRNA expression profiles of LTC and TIVE cells were generated by deep sequencing using Illumina HiSeq 2500. The mappable reads were aligned to the human genome and miRBase using Bowtie. Results: We show, through global cellular miRNA transcriptome analysis, that KSHV infection has a profound impact on the host miRNA expression landscape, up-regulating multiple miRNAs with oncogenic roles while down-regulating many tumor suppressive miRNAs, thereby contributing to KS oncogenesis. In particular, we identify miR-127-3p as one of the most significantly down-regulated miRNAs in LTC and restoring this miRNA inhibits KSHV-induced transformation, proliferation and tumorigenesis. Conclusions: This study provides a detailed analysis of the cellular miRNA transcriptome in LTC and TIVE cells using small RNA sequencing technology. We identify significant dysregulation of cellular miRNAs with important oncogenic or tumor-suppressive functions that may be physiologically relevant to KSHV oncogenesis. Moreover, our results identify a previously unrecognized tumor suppressor function for miR-127-3p in KS, indicating that its restoration offers potential as a therapeutic intervention for KS.

2021-11-01 | GSE158936 | GEO

Homo sapiens

Project description:AIDS-related Kaposi's sarcoma

| PRJNA85241 | ENA

AIDS-related Kaposi's sarcoma

Project description:Kaposi's Sarcoma (KS) is a proliferation of aberrant vascular structures lined by spindle cells, and is caused by a gammaherpes virus (HHV8/KSHV). Its course is aggravated by co-infection with HIV-1, where the timing of infection with HIV-1 and HHV8 is important for the clinical outcome. METHODS: In order to better understand the pathogenesis of KS, we have analysed tissue from two AIDS-KS lesions, and from normal skin by serial analysis of gene expression (SAGE). Semi-quantitative RT-PCR was then used to validate the results. RESULTS: The expression profile of AIDS-related KS (AIDS-KS) reflects an active process in the skin. Transcripts of HHV8 were found to be very low, and HIV-1 mRNA was not detected by SAGE, although it could be found using RT-PCR. Comparing the expression profile of AIDS-KS tissue with publicly available SAGE libraries suggested that AIDS-KS mRNA levels are most similar to those in an artificially mixed library of endothelial cells and leukocytes, in line with the description of KS lesions as containing spindle cells with endothelial characteristics, and an inflammatory infiltrate. At least 64 transcripts were found to be significantly elevated, and 28 were statistically downregulated in AIDS-KS compared to normal skin. Five of the upregulated mRNAs, including Tie 1 and sialoadhesin/CD169, were confirmed by semi-quantitative PCR to be elevated in additional AIDS-KS biopsies. Antibodies to sialoadhesin/CD169, a known marker of activated macrophages, were shown to specifically label tumour macrophages. CONCLUSION: The expression profile of AIDS-KS showed 64 genes to be significantly upregulated, and 28 genes downregulated, compared with normal skin. One of the genes with increased expression was sialoadhesin (CD169). Antibodies to sialoadhesin/CD169 specifically labelled tumour-associated macrophages, suggesting that macrophages present in AIDS-KS lesions belong to a subset of human CD169+ macrophages. Keywords: other

2003-07-16 | GSE514 | GEO

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