Microarray-based miRNA expression,identified miRNAs that were regulated by KSHV vIRF1
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA487803 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:HUVECs were transduced with lentiviral vIRF1 or control lentivirus (pHAGE),microarray-based miRNA expression profiling was adopted and identified a set of miRNAs that were differentially expressed between vIRF1- and pHAGE-transduced HUVECs
2018-08-25 | GSE119034 | GEO
Project description:Transcriptional profiling of BJAB cells transfected with KSHV miRNAs and BCBL cells treated with KSHV miRNA inhibitors. To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs often display small reductions in their steady-state levels, perhaps as a result of their impaired translation. Accordingly, we examined cellular transcript accumulation by array-based expression profiling under four sets of conditions in which KSHV miRNAs were expressed or inhibited.
2017-01-31 | GSE76472 | GEO
Project description:Purpose: Kaposi’s sarcoma associated-herpesvirus (KSHV) causes several hyperproliferative disorders, including Kaposi’s sarcoma, primary effusion lymphoma and multicentric Castleman’s disease. KSHV encodes for a number of microRNAs (miRNAs), and KSHV infection can affect the expression of cellular miRNAs. Hypoxia has been shown to induce KSHV reactivation, directly induce several KSHV lytic genes, and also induce the most abundant latent viral protein, LANA. Also, several KSHV proteins can stabilize and increase the cellular levels of hypoxia-inducible factor (HIF-1α). However, the degree to which hypoxic pathways are utilized by KSHV has yet to be determined. Methods: We investigated the interplay between hypoxia and KSHV infection by comparing the 31effects of hypoxia and KSHV infection on miRNA and mRNA expression, and by examining the 32effects of hypoxia on uninfected and KSHV-infected cells. This was accomplished using next-33generation sequencing (NGS), qRT-PCR, Taqman assays, and pathway analysis. Results: NGS analysis of human mRNAs revealed striking similarities (~34%) between the transcriptomic response to hypoxia and the transcriptomic response to KSHV infection. Additionally, hsa-miR-210, a key hypoxia-inducible miRNA with pro-angiogenic and anti-apoptotic properties, was found significantly up-regulated by both KSHV infection and hypoxia using Taqman assays. Finally, KSHV infected cells differed somewhat in their response to hypoxia compared to KSHV-uninfected controls. Conclusions: These results demonstrate that KSHV harnesses a part of the hypoxic cellular response and induces miR-210 up-regulation. The understanding of how these miRNAs, genes and pathways are regulated by HIF-1α and KSHV infection are essential to a better understanding of the biology of KSHV-associated diseases.
2016-12-21 | GSE79030 | GEO
Project description:Purpose: Kaposi’s sarcoma associated-herpesvirus (KSHV) causes several hyperproliferative disorders, including Kaposi’s sarcoma, primary effusion lymphoma and multicentric Castleman’s disease. KSHV encodes for a number of microRNAs (miRNAs), and KSHV infection can affect the expression of cellular miRNAs. Hypoxia has been shown to induce KSHV reactivation, directly induce several KSHV lytic genes, and also induce the most abundant latent viral protein, LANA. Also, several KSHV proteins can stabilize and increase the cellular levels of hypoxia-inducible factor (HIF-1α). However, the degree to which hypoxic pathways are utilized by KSHV has yet to be determined. Methods: We investigated the interplay between hypoxia and KSHV infection by comparing the 31effects of hypoxia and KSHV infection on miRNA and mRNA expression, and by examining the 32effects of hypoxia on uninfected and KSHV-infected cells. This was accomplished using next-33generation sequencing (NGS), qRT-PCR, Taqman assays, and pathway analysis. Results: NGS analysis of human mRNAs revealed striking similarities (~34%) between the transcriptomic response to hypoxia and the transcriptomic response to KSHV infection. Additionally, hsa-miR-210, a key hypoxia-inducible miRNA with pro-angiogenic and anti-apoptotic properties, was found significantly up-regulated by both KSHV infection and hypoxia using Taqman assays. Finally, KSHV infected cells differed somewhat in their response to hypoxia compared to KSHV-uninfected controls. Conclusions: These results demonstrate that KSHV harnesses a part of the hypoxic cellular response and induces miR-210 up-regulation. The understanding of how these miRNAs, genes and pathways are regulated by HIF-1α and KSHV infection are essential to a better understanding of the biology of KSHV-associated diseases.
2016-12-21 | GSE79029 | GEO
Project description:In the current study, we examined the cellular and viral miRNA expression profile in KSHV-infected patients without clinical signs of KSHV-associated disease. In addition, we characterized the viral miRNAs encoded by KSHV and EBV during natural infections in these patients. Finally, we show that malaria infection results in major alterations of the molecular content of plasma exosomes.
2018-02-16 | PXD008107 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below. Purpose: Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) causes several lymphoproliferative disorders, including KS, a common AIDS-associated malignancy. Cellular and viral microRNAs (miRNAs) have been shown to play important roles in regulating the expression of genes in oncogenesis. Herpesviruses, including KSHV, encode for miRNAs that are involved in angiogenesis, inflammation and apoptosis. A better knowledge of the miRNA-mediated pathways that regulate KSHV infection is therefore essential for an improved understanding of viral infection and pathogenesis. Methods: In this study, we used deep sequencing to analyze miRNA, both viral and human, and mRNA expression in KS tumor-derived human cells. Results: This approach revealed 153 differentially expressed human miRNAs between KSHV-positive and -negative cells. Differential expression of eight miRNAs was independently confirmed by qRT-PCR. We additionally showed that a majority (~73%) of KSHV-regulated miRNAs are down-regulated, including most members of the 14q32 miRNA cluster. Specifically, human miR-409-3p, which is known to target the pro-angiogenic growth factor angiogenin and the inflammation marker fibrinogen-beta, was significantly down-regulated in KSHV-infected cells based on deep sequencing and qRT-PCR. Despite this substantial down-regulation of cellular miRNAs, hsa-miR-708-5p was significantly up-regulated by KSHV and has been shown to directly inhibit pro-apoptotic protease Caspase-2. Finally, we evaluated to what extent there was an inverse correlation between miRNA and mRNA expression levels. Using filtered datasets, we identified relevant canonical pathways that were significantly enriched. Conclusion: Taken together, our data demonstrate that most human miRNAs affected by KSHV are repressed and our findings highlight the relevance of studying the post-transcriptional gene regulation of miRNAs for KSHV-associated malignancies.
2015-04-14 | GSE62829 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Purpose: Kaposi’s sarcoma (KS)-associated herpesvirus (KSHV) causes several lymphoproliferative disorders, including KS, a common AIDS-associated malignancy. Cellular and viral microRNAs (miRNAs) have been shown to play important roles in regulating the expression of genes in oncogenesis. Herpesviruses, including KSHV, encode for miRNAs that are involved in angiogenesis, inflammation and apoptosis. A better knowledge of the miRNA-mediated pathways that regulate KSHV infection is therefore essential for an improved understanding of viral infection and pathogenesis. Methods: In this study, we used deep sequencing to analyze miRNA, both viral and human, and mRNA expression in KS tumor-derived human cells. Results: This approach revealed 153 differentially expressed human miRNAs between KSHV-positive and -negative cells. Differential expression of eight miRNAs was independently confirmed by qRT-PCR. We additionally showed that a majority (~73%) of KSHV-regulated miRNAs are down-regulated, including most members of the 14q32 miRNA cluster. Specifically, human miR-409-3p, which is known to target the pro-angiogenic growth factor angiogenin and the inflammation marker fibrinogen-beta, was significantly down-regulated in KSHV-infected cells based on deep sequencing and qRT-PCR. Despite this substantial down-regulation of cellular miRNAs, hsa-miR-708-5p was significantly up-regulated by KSHV and has been shown to directly inhibit pro-apoptotic protease Caspase-2. Finally, we evaluated to what extent there was an inverse correlation between miRNA and mRNA expression levels. Using filtered datasets, we identified relevant canonical pathways that were significantly enriched. Conclusion: Taken together, our data demonstrate that most human miRNAs affected by KSHV are repressed and our findings highlight the relevance of studying the post-transcriptional gene regulation of miRNAs for KSHV-associated malignancies.
2015-04-14 | GSE62828 | GEO
Project description:Micro (mi)RNAs are small non-coding RNAs with key regulatory functions. Recent advances in the field allowed researchers to identify their targets. However, much less is known regarding the regulation of miRNA themselves. The accumulation of these tiny regulators can be modulated at various levels during their biogenesis from the transcription of the primary transcript (pri-miRNA) to the stability of the mature miRNA. Here, we studied the importance of the pri-miRNA secondary structure for the regulation of mature miRNAs accumulation. To this end, we used the KaposiM-bM-^@M-^Ys sarcoma herpesvirus, which encodes a cluster of twelve pre-miRNAs. Using small RNA profiling and quantitative northern blot analysis, we measured the absolute amount of each mature miRNAs in different cellular context. We found that the difference in expression between the least and most expressed viral miRNA could be as high as 60-fold. Using high-throughput selective 2M-bM-^@M-^Y-hydroxyl acylation analyzed by primer extension (hSHAPE), we then determined the secondary structure of the long primary transcript. We found that highly expressed miRNAs derived from optimally structured regions within the pri-miRNA. Finally, we confirmed the importance of the local structure by swapping stem-loops for highly and lowly expressed miRNAs, which resulted in a perturbed accumulation of the mature miRNA. Examination of sRNA profiles in 3 independent B cell lines expressing KSHV miRNAs or infected with KSHV, without replicate
2014-06-02 | E-GEOD-53296 | biostudies-arrayexpress
Project description:Transcriptional profiling of HUVECs transfected with KSHV miRNA mimics (vMix) or a negative control mimic (neg). To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs can display small reductions in their steady-state levels. Cells transfected with negative control miRNA compared to cells transfected with KSHV miRNAs. Experimental treatment versus control treatment
2014-09-01 | E-GEOD-43640 | biostudies-arrayexpress
Project description:Transcriptional profiling of HUVECs transfected with KSHV miRNA mimics (vMix) or a negative control mimic (neg). To identify host RNA targets of KSHV miRNAs, we took advantage of the observation that RNAs targeted by miRNAs can display small reductions in their steady-state levels.
2014-09-01 | GSE43640 | GEO