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

ABSTRACT: Genome-wide transcriptome analysis of KSHV long-term-infected endothelial (LTC) and parental uninfected TIVE cells [RNA-seq]

PROVIDER: PRJNA667058 | ENA |

REPOSITORIES: ENA

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

Project description:Purpose: To characterize genome-wide mRNA 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: mRNA expression profiles of LTC and TIVE cells were generated by deep sequencing using Illumina. In addition, mRNA profiles of LTC transfected with miR-127-3p or negative control (NC) mimic were generated by deep sequencing. Results: We analyzed global transcriptome changes in LTC compared to TIVE cells and identified significant upregulation of many cell cycle and oncogenic signaling pathways. In addition, we assessed global transcriptome changes in LTC transfected with miR-127-3p mimic and found a significant decrease in the levels of E2F and Myc targets, indicating that miR-127-3p suppresses E2F and Myc transcriptional activities. Conclusions: This study provides a detailed analysis of the cellular transcriptome in LTC and TIVE cells using RNA sequencing technology. Our study identifies miR-127-3p as a potent tumor suppressor miRNA that acts as a negative regulator of the CDK-RB-E2F cell cycle signaling pathway and the oncogenic Myc network in the context of KSHV oncogenesis and establishes a strong rationale for developing this miRNA as a therapeutic agent against KS.

2021-11-01 | GSE158935 | GEO

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

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

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

| PRJNA667057 | ENA

KSHV-infected invasive bladder cancer cell: Control vs. KSHV-infected

Project description:Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells. Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells.

2015-03-10 | E-GEOD-66682 | biostudies-arrayexpress

KSHV-infected invasive bladder cancer cell: Control vs. KSHV-infected

Project description:Transcriptional profiling of bladder cancer cell lines comparing control uninfected cells with KSHV-infected cells.

2015-03-10 | GSE66682 | GEO

Mock or KSHV cells (BJABJ, BCBL, TIME and HUVEC) vs common reference (mixture of RNA from both infected and uninfected cells)

Project description:Expression profiling of latently infected cells using a custom tiling microarray HUVEC and TIME cells were infected BCBL-1-derived KSHV. Mock infected HUVEC and TIME cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. KSHV-infected cells are induced to enter lytic cycle with valproate or Adenovirus-RTA. Cells were harvested at indicated time points and analyzed. Three condition experiment: mock infected, latently infected cells and lytically infected. Three cell types (BJAB cells served as uninfected controls for the BCBL-1 cells).

2010-07-07 | E-GEOD-21972 | biostudies-arrayexpress

Mock or KSHV cells (BJABJ, BCBL, TIME and HUVEC) vs common reference (mixture of RNA from both infected and uninfected cells)

2010-07-07 | GSE21972 | GEO

KSHV regulation of gene expression in the human endothelial cell line EAHY

2011-11-29 | GSE33984 | GEO

KSHV regulation of gene expression in the human endothelial cell line EAHY

Project description:KSHV promotes endothelia to mesenchymal transformation (EntMT) in EAHY cells We have used Affymetrix Gene Arrays to investigate the patterns of regulation of gene expression in EAHY cells infected with KSHV in comparison to uninfected EAHY cells EAHY cells were infected with rKSHV.219 virus (derived from the virus-producing VERO cells). 12 days after infection and in puromycin selection to achieve greater than 90% infection RNA was exctrated from KSHV infected and control non-infected cells.

2011-11-29 | E-GEOD-33984 | biostudies-arrayexpress

KSHV uses viral IL6 to expand infected immunosuppressive macrophages (scRNA-seq)

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is an oncogenic double-stranded DNA virus and the etiologic agent of Kaposi’s sarcoma and hyperinflammatory lymphoproliferative disorders. Understanding the mechanism by which KSHV increases infected cell populations is crucial for curing KSHV-associated diseases. Here, we demonstrate that KSHV preferentially infects CD14+ monocytes and sustains viral replication through the viral interleukin-6 (vIL-6)-mediated activation of STAT1 and 3. Using vIL6-sufficient and vIL6-deficient recombinant KSHV, we demonstrated that vIL6 plays a critical role in promoting the proliferation and differentiation of KSHV-infected monocytes into macrophages. The macrophages derived from vIL6-sufficient (wild type) KSHV infection showed a distinct transcriptional profile of elevated IFN-pathway activation with immune suppression and were compromised in T-cell stimulation function compared to those from vIL6-deficient KSHV infection or uninfected control. These results highlight a clever strategy, in which KSHV utilizes vIL6 to secure its initial viral pool by expanding infected dysfunctional macrophages. This mechanism also facilitates KSHV to escape from host immune surveillance and to establish a lifelong infection.

2023-08-30 | GSE227166 | GEO

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