High-throughput mRNA sequencing and microRNA sequencing analysis of human nasopharyngeal carcinoma cell line (6-10B) transfected with EBV-encoded microRNA BART2-5p mimics
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909162 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22543440.fastq.gz | Fastqsanger.gz | |||
| SRR22543441.fastq.gz | Fastqsanger.gz | |||
| SRR22543442.fastq.gz | Fastqsanger.gz | |||
| SRR22543443.fastq.gz | Fastqsanger.gz | |||
| SRR22543444_1.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are using mRNA and microRNA sequencing analysis to evaluate the effects of EBV-encoded microRNA BART2-5p mimics on the mRNA and microRNA profiles of human nasopharyngeal carcinoma cell line 6-10B. Methods: 6-10B cells were transfected with either EBV microRNA BART2-5p mimics or negative control (NC) mimics for 48 hours. Cellular RNA was then sequenced at the mRNA and microRNA levels using illumina high-throughput sequencing service (Oebiotech, Shanghai, China). Data were extracted and normalized according to the manufacturer's standard protocol. Results: Log-fold changes of up- or down-regulated mRNAs and microRNAs between the control and experiment group were selected with a significance threshold of p<0.05. Conclusions: Our study describes the mRNA and microRNA alterations induced by EBV-miRNA-BART2-5p in 6-10B cells
2023-09-14 | GSE220166 | GEO
Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are using transcriptome profiling (RNA-seq) to evaluate the effects of EBV infection or (and) EBV BART6-3p mimics on the global transcriptome of the BJAB cells. Methods: BJAB cells were transfected with negative control mimics or BART6-3p mimics for 48 h and then infected with EBV virons for 2h. RNAs were extracted by Trizol and sequenced by Solexa high-throughput sequencing service (Oebiotech, Shanghai, China). Data were extracted and normalized according to the manufacturer’s standard protocol. Results: Log-fold changes of up- or down-regulated mRNAs between the control and experiment group were selected with a significance threshold of p<0.05. There are 408 mRNAs were up-regulated and 263 were down-regulated in “EBV infection” group cells comparing to “Mock” group cells. There are 385 mRNAs were up-regulated and 246 were down-regulated in “EBV infection + Bart6-3p mimics” group cells comparing to “EBV infection + negative control mimics” group cells. Conclusions: Our study describes the global transciptome changes of BJAB cells induced by EBV infection or (and) EBV 6-3p mimics.
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Project description:The Epstein Barr virus (EBV) encoded latent membrane protein-1 (LMP1) is a functional homologue of the tumor necrosis factor receptor family and contributes substantially to the oncogenic potential of EBV through activation of Nuclear Factor-kappaB (NF-kappaB). MicroRNAs (miRNAs) are a class of small RNA molecules that are involved in the regulation of cellular processes such as growth, development, and apoptosis, and have recently been linked to cancer phenotypes. Through miRNA microarray analysis, we demonstrate that LMP1 dysregulates the expression of several cellular miRNAs, including the most highly regulated of these, miR-146a. Quantitative RT-PCR analysis confirmed induced expression of miR-146a by LMP1. Analysis of miR-146a expression in EBV latency type III and type I cell lines revealed substantial expression of miR-146a in type III (which express LMP1) but not in type I cell lines. Reporter studies demonstrated that LMP1 induces miR-146a predominantly through two NF-kappaB binding sites in the miR-146a promoter and identified a role for an OCT-1 site in conferring basal and induced expression. Array analysis of cellular mRNAs expressed in Akata cells transduced with an miR-146a expressing retrovirus identified genes that are directly or indirectly regulated by miR-146a, including a group of interferon responsive genes that are inhibited by miR-146a. Since miR-146a is known to be induced by agents that activate the interferon response pathway (including LMP1), these results suggest that miR-146a functions in a negative feedback loop to modulate the intensity and/or duration of the interferon response. Keywords: microRNA expression modified by EBV encoded oncogene, LMP1 EBV negative Mutu E1dn Cl. 3 cells were transduced with either a control retrovirus (pEhyg) or an LMP1 containing retrovirus (pEhyg-FLAG-LMP1). Cells were selected with hygromycin for approximately 2 weeks afterwhich 5 pairs of RNA preps were carried out on 5 successive days. Arrays GSM255656 and GSM255659 are dye swaps in which LMP1 samples were labeled with Cy3 and control samples were labeled with Cy5.
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Project description:In EBV-associated tumors, such as gastric cancer (GC) and Burkitt’s lymphoma (BL), a high proportion of microRNAs are virally encoded. To explore the targets of both viral and host microRNAs, we performed Crosslinking, Ligation, and Sequencing of Hybrids (CLASH). With this approach, we were able to quantify each Argonaute-bound microRNA-mRNA interaction in a GC (SNU719), and BL (Akata) cell line.
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Project description:MicroRNA-10b may target numerous genes in gliomagenesis. The target genes of miR-10b may differ according to the cellular context. We used microarray analyses to determine the phenotypic effects and gene targets of miR-10b by silencing miR-10b in invasive U87-2M1 glioma cells.
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2021-11-03 | GSE181922 | GEO
Project description:Background/ Aim: Diabetes has substantive co-occurrence with disorders of gut-brain interactions (DGBIs). The pathophysiological and molecular mechanisms linking diabetes and DGBIs are unclear. miRNAs are key regulators of diabetes and gut dysmotility. We investigated whether impaired gut barrier function regulated by a key miRNA, miR-10b-5p, links diabetes and gut dysmotility. Methods: We created a new mouse line using the Mb3Cas12a/Mb3Cpf1 endonuclease to knock out mir-10b globally. Loss of function studies were conducted to characterize diabetes, gut dysmotility, and gut barrier dysfunction phenotypes in these mice. Gain of function studies were conducted by injecting these mice with a miR-10b-5p mimic. Further, we performed miRNA-sequencing analysis from colonic mucosa from mir-10b KO, WT, and miR-10b-5p mimic injected mice to confirm 1) deficiency of miR-10b-5p in KO mice, and 2) restoration of miR-10b-5p expression after the mimic injection. Results: Congenital loss of mir-10b in mice led to the development of hyperglycemia, gut dysmotility, and gut barrier dysfunction. We found increased gut permeability and reduced expression of the tight junction protein Zonula occludens-1 (ZO-1), in the colon of mir-10b KO mice. We further confirmed that patients with diabetes or IBS-C, a known DGBI that is linked to leaky gut, had significantly reduced miR-10b-5p expression. Injection of a miR-10b-5p mimic in mir-10b KO mice rescued these molecular alterations and phenotypes. Conclusion: Our study uncovered a potential pathophysiologic mechanism of gut barrier dysfunction that links both the diabetes and gut dysmotility phenotypes in mice lacking miR-10b-5p. Treatment with a miR-10b-5p mimic reversed the leaky gut, diabetic, and gut dysmotility phenotypes, highlighting the translational potential of miR-10b-5p mimic.
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