Regulation network and expression profiles of Epstein-Barr virus-encoded microRNAs and their potential target host genes in nasopharyngeal carcinomas

Zeng, Zhaoyang; Huang, Huichao; Huang, Lili; Sun, Mengxi; Yan, Qijia; Song, Yali; Fang, Wei; Bo, Hao; Gong, Zhaojian; Zeng, Yong; Li, Qiao; Zhang, WenLing L.; Li, XiaYu Y.; Xiang, Bo; Li, XiaoLing L.; Li, Yong; Wang, Xiong; Li, Guiyuan

doi:10.1007/s11427-013-4577-y

Cited by 67 publications

(57 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The average of three independent analyses for each gene was calculated. The fold changes were calculated through relative quantification ð2 ÀDDC t Þ [29]. All reactions were run in triplicate and repeated in three independent experiments.…”

Section: Qrt-pcrmentioning

confidence: 99%

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Xiong

Zhou

et al. 2015

Mol Cell Biochem

Self Cite

View full text Add to dashboard Cite

BRD7 is a single bromodomain-containing protein that functions as a subunit of the SWI/SNF chromatin-remodeling complex to regulate transcription. It also interacts with the well-known tumor suppressor protein p53 to trans-activate genes involved in cell cycle arrest. In this paper, we report an integrative analysis of genome-wide chromatin occupancy of BRD7 by chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) and digital gene expression (DGE) profiling by RNA-sequencing upon the overexpression of BRD7 in human cells. We localized 156 BRD7-binding peaks representing 184 genes by ChIP-sequencing, and most of these peaks were co-localized with histone modification sites. Four novel motifs were significantly represented in these BRD7-enriched regions. Ingenuity pathway analysis revealed that 22 of these BRD7 target genes were involved in a network regulating cell death and survival. DGE profiling identified 560 up-regulated genes and 1088 down-regulated genes regulated by BRD7. Using Gene Ontology and pathway analysis, we found significant enrichment of the cell cycle and apoptosis pathway genes. For the integrative analysis of the ChIP-seq and DEG data, we constructed a regulating network of BRD7 downstream genes, and this network suggests multiple feedback regulations of the pathways. Furthermore, we validated BIRC2, BIRC3, TXN2, and NOTCH1 genes as direct, functional BRD7 targets, which were involved in the cell cycle and apoptosis pathways. These results provide a genome-wide view of chromatin occupancy and the gene regulation network of the BRD7 signaling pathway.

show abstract

Section: Qrt-pcrmentioning

confidence: 99%

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Xiong

Zhou

et al. 2015

Mol Cell Biochem

Self Cite

View full text Add to dashboard Cite

show abstract

“…Accumulating evidence has shown that they play crucial roles in many physiological processes, such as carcinogenesis, by modulating gene expression at the epigenetic, transcriptional and posttranscriptional levels [11–15]. Furthermore, recent studies have identified multiple functional effects of lncRNAs involving in various cellular processes, such as tumor initiation, progression and metastasis, and the dysregulation of lncRNAs are a primary feature of some human cancers [16–19]. At the same time, a great quantity identified results revealed that lncRNAs play an important role in pathogenesis of head and neck cancers [20–22].…”

Section: Introductionmentioning

confidence: 99%

Overexpression long non-coding RNA LINC00673 is associated with poor prognosis and promotes invasion and metastasis in tongue squamous cell carcinoma

Liu

Gong

et al. 2016

Oncotarget

Self Cite

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) associated with the tumorigenesis of human cancers. However, the relevance of lncRNAs in tongue squamous cell carcinoma (TSCC) is still unclear. To discover novel TSCC-related lncRNAs, we analyzed the lncRNA expression patterns in two sets of TSCC gene expression profile data, and found that long intergenic non-coding RNA 673 (LINC00673) was significantly upregulated in TSCC samples. Then we examined LINC00673 expression in 202 TSCC tissue specimens, LINC00673 is highly expressed in a significant proportion of human TSCC biopsies and correlates with poor prognosis. Knockdown LINC00673 significantly inhibited the cell invasion and migration capability in TSCC cells. Our findings suggest that LINC00673 may play an essential role in TSCC progression and might serve as a potential biomarker for early detection and prognosis prediction of TSCC.

show abstract

“…EBV encodes 44 mature microRNAs (miRNAs), divided into two clusters, BHRFs and BARTs [14–16]. BART miRNAs were shown to affect the malignant phenotype of some lymphomas [17], GC [18], and NPC [19–22], including viral latency [23–25], immune escape [26], cell proliferation [27], cell apoptosis [28, 29], cell cycle regulation, and cancer metabolism [27–30]. These findings suggest that EBV miRNAs may exert a variety of important regulatory functions in EBV-mediated tumorigenesis and cancer progression.…”

Section: Introductionmentioning

confidence: 99%

Epstein-Barr virus encoded miR-BART11 promotes inflammation-induced carcinogenesis by targeting FOXP1

Song

Zeng

et al. 2016

Oncotarget

Self Cite

View full text Add to dashboard Cite

Epstein-Barr virus (EBV) infection and chronic inflammation are closely associated with the development and progression of nasopharyngeal carcinoma (NPC) and gastric cancer (GC), and the infiltration of inflammatory cells, including tumor-associated macrophages (TAMs), is often observed in these cancers. EBV encodes 44 mature micro RNAs (miRNAs), but the roles of only a few EBV-encoded miRNA targets are known in cancer development, and here, our aim was to elucidate the effects of EBV-miR-BART11 on FOXP1 expression, and potential involvement in inflammation-induced carcinogenesis. We constructed an EBV miRNA-dependent gene regulatory network and predicted that EBV-miR-BART11 is able to target forkhead box P1 (FOXP1), a key molecule involved in monocyte to macrophage differentiation. Here, using luciferase reporter assay, we confirmed that EBV-miR-BART11 directly targets the 3′-untranslated region of FOXP1 gene, inhibits FOXP1 induction of TAM differentiation, and the secretion of inflammatory cytokines into the tumor microenvironment, inducing the proliferation of NPC and GC cells. FOXP1 overexpression hindered monocyte differentiation and inhibited NPC and GC cells growth. Our results demonstrated that EBV-miR-BART11 plays a crucial role in the promotion of inflammation-induced NPC and GC carcinogenesis by inhibiting FOXP1 tumor-suppressive effects. We showed a novel EBV-dependent mechanism that may induce the carcinogenesis of NPC and GC, which may help define new potential biomarkers and targets for NPC and GC diagnosis and treatment.

show abstract

Regulation network and expression profiles of Epstein-Barr virus-encoded microRNAs and their potential target host genes in nasopharyngeal carcinomas

Cited by 67 publications

References 62 publications

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Integrating ChIP-sequencing and digital gene expression profiling to identify BRD7 downstream genes and construct their regulating network

Overexpression long non-coding RNA LINC00673 is associated with poor prognosis and promotes invasion and metastasis in tongue squamous cell carcinoma

Epstein-Barr virus encoded miR-BART11 promotes inflammation-induced carcinogenesis by targeting FOXP1

Contact Info

Product

Resources

About