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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RNA-seq]

ABSTRACT: RNA-seq technology was used to investigate the differentially expressed genes and regulated alternative splicing events in Kaposi's sarcoma lesions and adjacent non-tumor tissues. We then performed gene expression profiling analysis using data obtained from RNA-seq.

ORGANISM(S): Homo sapiens

PROVIDER: GSE212961 | GEO | 2023/10/20

REPOSITORIES: GEO

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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma [RIP-seq]

Project description:In order to clarify the post-transcriptional regulatory network of RPS27 in KS. We constructed a transcriptomic binding network using iRIP-seq. The KS lesions of the other two patients were used for separately.

2023-10-20 | GSE212960 | GEO

Epigenetic reprogramming of Kaposi’s sarcoma-associated herpesvirus during hypoxic reactivation

Project description:Chromatin Immuno-precipitaion sequencing was performed using H3-Ac, H3K4Me3, H3K9Me3, H3K27Me3, LANA, RTA and DNA Polymerase 1 alpha antibodies to investigate its enrichment on Kaposi's sarcoma associated herpesvirus (KSHV) genome in BC3 cells under normoxic or hypoxic conditions

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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.

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RNA-binding protein RPS27 and gene expression regulation in Kaposi’s sarcoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-20 | GSE212962 | GEO

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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.

2023-07-14 | GSE222527 | GEO

RNA-Seq of Kaposi’s sarcoma reveal alterations in glucose and lipid metabolism

Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiologic agent of Kaposi’s sarcoma (KS). In sub-Saharan Africa, the high prevalence of both HIV-1 and KSHV has made KS a leading cancer in the region, associated with poor prognosis and high mortality due to late medical presentation and advanced disease stages. A better understanding of the cellular and viral transcriptome profiles during neoplastic growth will aid in the definition of biomarkers and cellular functions associated with KS tumorigenesis and progression. Our approach is to examine the transcriptome profile in actual KS lesions versus non-cancer tissues from the same individual for a total of four male African epidemic KS patients. These patients have undetectable HIV-1 plasma viral load after successful anti-retroviral therapy. Our results capture the cellular complexity of in vivo lesion environment and provide a marked contrast to those derived from in vitro monoculture models. The findings demonstrate that latency and immune modulation related functions dominate the viral gene expression pattern. Moreover, KSHV significantly affected the cellular transcriptome profile with genes involved in lipid and glucose metabolism disorder pathways being the most substantially dysregulated. Despite the implied infiltration of immune cells into the lesions as predicted by CIBERSORT, KS tumor continued to progress, suggesting immunological dysfunction in these KS patients despite control of HIV-1 viremia. Lastly, there is limited overlap of our in vivo dataset with in vitro studies, suggesting a limitation of in vitro KS models.

2018-01-17 | GSE100684 | GEO

Kaposi's sarcoma-associated herpes virus

Project description:Primary human dermal endothelial cells were infected or NOT infected with isolated Kaposi's sarcoma associated herpes virus for 7 days. Total RNA was isolated using Trireagent and subjected to microarray. Keywords: other

2004-05-08 | GSE1377 | GEO

Transcription profiling of human primary dermal endothelial cells infects with Kaposis sarcoma-associated herpes virus vs. controls

2008-06-12 | E-GEOD-1377 | biostudies-arrayexpress

Apoptosis regulation by Kaposi’s sarcoma microRNAs

Project description:Herpesviruses are known to encode micro (mi)RNAs and to use them to regulate the expression of both viral and cellular genes. The genome of Kaposi’s sarcoma herpesvirus (KSHV) encodes a cluster of twelve miRNAs, which are abundantly expressed during both latency and lytic infection. Relatively few cellular targets of KSHV miRNAs are known. Here, we used a microarray expression profiling approach to analyze the transcriptome of both B lymphocytes and endothelial cells stably expressing KSHV miRNAs and monitor the changes induced by the presence of these miRNAs. We generated a list of potential cellular targets by looking for miRNA seed-match-containing transcripts that were significantly down regulated upon KSHV miRNAs expression. Interestingly, the overlap of putative targets identified in B lymphocytes and endothelial cells was minimal, suggesting a tissue-specific target-regulation by viral miRNAs. Among the putative targets, we identified caspase 3, a critical factor for the control of apoptosis, which we validated using luciferase reporter assays and western blotting. In functional assays we obtained further evidence that KSHV miRNAs indeed protect cells from apoptosis. Single-channel hybridization to Affymetrix oligonucleotides microarrays. DG75 and EA.hy926 cells were transducted in triplicates with the K10/12 and K12/12 lentiviral constructs expressing the KSHV miRNAs, or with a GFP-expressing construct as control. The K10/12 construct expressed only the ten intronic miRNAs miR-K12-1 to 9 and miR-K12-11 while the K12/12 construct also expressed miR-K12-10 and miR-K12-12 in addition.

2011-10-27 | E-GEOD-18946 | biostudies-arrayexpress

RNA-seq of two Kaposi’s sarcoma tissue samples and the corresponding two normal tissue samples

Project description:We have reported that KSHV infection reprograms oral mesenchymal stem cells (MSCs) and transforms them to Kaposi sarcoma-like cells through mesenchymal-to-endothelial transition. To explore the mechanism of KSHV infection of MSCs, we compared the gene expression profiles of Kaposi’s sarcoma tissue and KSHV non-susceptible cells to explore potential host factors that contribute to KSHV infection.

2023-02-28 | GSE201321 | GEO

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