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(A) Cis-regulation of the networks. Red spot represented differential expression of lncRNA. Blue spot represented cis-regulation gene. (B) Trans-regulation of the networks. Red spot represented differential expression of lncRNA. Blue spot represented trans-regulation gene.
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Background: Little knowledge about long non-coding RNAs(lncRNAs) in nasopharyngeal carcinoma (NPC) has been acquired.
Methods: Next-generation sequencing was applied in 7 cases of NPC tissues and 7 cases of normal tissues in nasopharynx. PLEX, CNCI and CPAT soft-wares were used to predict novel lncRNAs. Real-time Quantitative PCR (qPCR) further val...
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Cystic echinococcosis is a worldwide chronic zoonotic disease caused by infection with the larval stage of Echinococcus granulosus. Previously, we found significant accumulation of myeloid-derived suppressor cells (MDSCs) in E. granulosus infection mouse models and that they play a key role in immunosuppressing T lymphocytes. Here, we...
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... et al. have found that CTA-398F10.2 can be increased by radiation in glioma cells but not in normal astrocytes[36]. Li et al. have found that the proto-oncogene JUN is correlated with RP4-794H19.1 and contributes to TNF signaling pathway in nasopharyngeal cancer[37]. James et al. have found that RP11-677M14.3 is associated with the different molecular subtypes of B cell acute lymphoblastic leukemia and co-occurrent with TGFB2 expression[38]. ...
This study aimed to explore the prognostic and predictive value of autophagy-related lncRNAs in papillary thyroid carcinoma (PTC). The expression data of autophagy-related genes and lncRNAs of the PTC patients were obtained from TCGA database. Autophagy-related-differentially expressed lncRNAs (DElncs) were identified and used to establish the lncRNAs signature predicting patients’ progression-free interval (PFI) in the training cohort. Its performance was assessed in the training cohort, validation cohort, and entire cohort. Effects of the signature on I-131 therapy were also explored. We identified 199 autophagy-related-DElncs and constructed a novel six-lncRNAs signature was constructed based on these lncRNAs. This signature had a good predictive performance and was superior to TNM stages and previous clinical risk scores. I-131 therapy was found to be associated with favorable prognosis in patients with high-risk scores but not those with low-risk scores. Gene set enrichment analysis suggested that a series of hallmark gene sets were enriched in the high-risk subgroup. Single-cell RNA sequencing analysis suggested that the lncRNAs were mainly expressed in thyroid cells but not stromal cells. In conclusion, our study constructed a well-performed six-lncRNAs signature to predict PFI and I-131 therapy benefits in PTC.
... There is evidence that lncRNA disorders are involved in cell transformation and development of a variety of cancers, including NPC [14,15]. Through microarray and high-throughput RNA sequencing, a large number of lncRNAs have been identified in NPC tissues and cell lines [16]. One of the main mechanisms for tumours to "educate" platelets is through tumour-derived extracellular vesicles, which are captured by the platelets and ultimately lead to abnormal RNA profiles, including those of lncRNAs [17]. ...
Early diagnosis is essential for the treatment and prevention of nasopharyngeal cancer. However, there is a lack of effective biological indicators for nasopharyngeal carcinoma (NPC). Therefore, we explored the potential biomarkers in tumour-educated blood platelet (TEP) RNA in early NPC. Platelets were isolated from blood plasma and their RNA was extracted. High-throughput sequenced data from a total of 33 plasma samples were analysed using DESeq2 to identify the differentially expressed genes (DEGs). Subsequently, the DEGs were subjected to principal component analysis (PCA), gene ontology (GO) analysis, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis; and Cytoscape, TargetScan, and miRanda software were used for inferring the competing endogenous RNA network. We identified 19 long non-coding (lnc) RNAs (DElncRNAs) and 248 mRNAs (DEmRNAs) that were differentially expressed in the TEP RNA. In addition, SELP gene mRNA and lncRNAs AC092135.3, AC012358.2, AL021807.1, AP001972.5, and GPX1 were found to be down-regulated DEmRNA and DElncRNAs in the early stage of NPC. Bioinformatic analysis showed that these DEmRNAs and DElncRNAs may be involved in regulating the pathogenesis of NPC. Our research may provide new insights for exploring the biological mechanisms of NPC and early diagnosis using potential biomarkers.
... As mentioned above, compared with normal nasal mucosa, there are a large number of unusual levels of lncRNAs in NPC tissues, which are helpful to distinguish NPC patients from normal people. The Genome sequencing showed that 306 lncRNAs are up-regulated, while 204 lncRNAs are down regulated [138]. Although only a few known lncRNAs have function annotation. ...
Nasopharyngeal carcinoma (NPC) is a kind of malignant tumor with ethnic and geographical distribution characteristics. However, the molecular mechanisms of NPC are still unclear. Long non encoding RNAs (lncRNAs) are becoming important regulators in gene expression networks, including post transcriptional and post translational regulation of protein, protein complex organization, signal transduction and recombination among cells, which are involved in cancer recognition. Recent evidence shows that lncRNAs play important roles in the occurrence and development of NPC. Therefore, in-depth understanding of abnormal lncRNAs will provide new understanding of the pathogenesis in NPC, and provide new tools for the early diagnosis and treatment of NPC. This article reviews the abnormal lncRNAs in NPC cells and the roles of lncRNAs in the tumorigenesis of NPC. In addition, we also discuss the diagnostic and therapeutic potential of lncRNAs in NPC.
... Meanwhile, we found that higher CASC9 expression was positively correlated with advanced TNM stage and shorter overall survival in HNSC (P=0.0315 and P=0.016, Figures 1C, D). To confirm the discovery in HNSC, we identified DElncRNAs in NPC and found that expression of CASC9 was similarly higher in NPC compared with normal tissues based on two independent NPC RNA-seq datasets ( Figure 1E and Supplementary Tables 4, 5) (19,20). By reviewing literatures, we discovered that CASC9-related researches is still very limited and the role of CASC9 in tumor progression remains unknown. ...
Nasopharyngeal carcinoma (NPC) is a major kind of head and neck epithelial carcinoma. Increasing evidences reveal that long noncoding RNAs are considered as vital regulators in tumorigenesis and progression. Although previous studies have found that cancer susceptibility candidate 9 (CASC9) highly expresses in NPC, the underlying mechanisms need to be further studied. In this study, we found that CASC9 was overexpressed and associated with worse prognosis in NPC. CASC9 knockdown significantly inhibited the cell proliferation, migration and invasion in vitro and enhanced the sensitivity of tumor cells to cisplatin and paclitaxel. Mechanism research confirmed CASC9 regulated the malignant biological behavior of nasopharyngeal carcinoma cells by targeting miR-497-5p/Wnt3a/β-catenin signaling pathway. The present study might provide a novel mechanism for tumorigenesis and progression of NPC and contribute to the development of an effective molecular target therapy.
... NR2F2-AS1 was also significantly down-regulated in lung adenocarcinoma tissues both in the TCGA dataset and qRT-PCR experiment [27]. In addition, the results of next-generation sequencing and qPCR validated that NR2F2-AS1 was downregulated in nasopharyngeal carcinoma [28]. In the present study, we observed that the expression of NR2F2-AS1 was down-regulated in CRC and inversely correlated with the level of miR-106b. ...
Increasing numbers of miRNAs have been observed as oncogenes or tumor suppressors in colorectal cancer (CRC). It was recently reported that hsa-miR-106b-5p (miR-106b) promoted CRC cell migration and invasion. However, there were also studies showing contradictory results. Therefore, in the present study, we further explore the role of miR-106b and its downstream networks in the carcinogenesis of CRC. We observed that the expression of miR-106b is significantly increased in Pan-Cancer and CRC tissues compared with normal tissues from The Cancer Genome Atlas (TCGA) database. Furthermore, we used Transwell, Cell Counting Kit-8, and colony formation assays to clarify that miR-106b promotes the migratory, invasive, and proliferative abilities of CRC cells. For the first time, we systematically screened the target mRNAs and lncRNAs of miR-106b using TCGA database and the bioinformatics algorithms. Dual-luciferase reporter assay confirmed that NR2F2-AS1 and PLEKHO2 are the direct targets of miR-106b. Furthermore, NR2F2-AS1 acts as a competing endogenous RNA (ceRNA) to regulate PLEKHO2 expression by sponging miR-106b. The results of Gene set enrichment analysis (GSEA) and Western blot indicated that they play important roles in CRC progression by regulating MAPK pathway. Thus, miR-106b/NR2F2-AS1/PLEKHO2/MAPK signaling axis may suggest the potential usage in CRC treatment.
... Li et al. based on next-generation sequencing (NGS) analysis, suggested that 62 lncRNAs trans-regulated genes participate in the EBV infection pathway and that the proto-oncogene JUN was related to the cis-regulatory lncRNA RP4-794H19.1 and contributes to the tumour necrosis factor (TNF) signalling pathway in NPC, although these ideas need further practical validation [97]. Additionally, NGS, a high-throughput technique based on massive, small reads of the genome, enables rapid sequencing of the base pairs in DNA or RNA samples and the genomics data come from Whole Exome Sequencing (WES) and RNA sequencing (RNAseq). ...
Epstein Barr-virus (EBV) is related to several cancers. Long non-coding RNAs (lncRNAs) act by regulating target genes and are involved in tumourigenesis. However, the role of lncRNAs in EBV-associated cancers is rarely reported. Understanding the role and mechanism of lncRNAs in EBV-associated cancers may contribute to diagnosis, prognosis and clinical therapy in the future. EBV encodes not only miRNAs, but also BART lncRNAs during latency and the BHLF1 lncRNA during both the latent and lytic phases. These lncRNAs can be targeted regulate inflammation, invasion, and migration and thus tumourigenesis. The products of EBV also directly and indirectly regulate host lncRNAs, including LINC00312, NORAD CYTOR, SHNG8, SHNG5, MINCR, lncRNA-BC200, LINC00672, MALATI1, LINC00982, LINC02067, IGFBP7‐AS1, LOC100505716, LOC100128494, NAG7 and RP4-794H19.1, to facilitate tumourigenesis using different mechanisms. Additionally, lncRNAs have been previously validated to interact with microRNAs (miRNAs), and lncRNAs and miRNAs mutually suppress each other. The EBV-miR-BART6-3p/LOC553103/STMN1 axis inhibits EBV-associated tumour cell proliferation. Additionally, H. pylori –EBV co-infection promotes inflammatory lesions and results in EMT. HPV–EBV co-infection inhibits the transition from latency to lytic replication. KSHV–EBV co-infection aggravates tumourigenesis in huNSG mice. COVID-19–EBV co-infection may activate the immune system to destroy a tumour, although this situation is rare and the mechanism requires further confirmation. Hopefully, this information will shed some light on tumour therapy strategies tumourigenesis. Additionally, this strategy benefits for infected patients by preventing latency to lytic replication. Understanding the role and expression of lnRNAs in these two phases of EBV is critical to control the transition from latency to the lytic replication phase. This review presents differential expressed lncRNAs in EBV-associated cancers and provides resources to aid in developing superior strategies for clinical therapy.
... THAP9 antisense RNA 1 (THAP9-AS1), a lncRNA located on 4q21.22, was previously discovered to be upregulated in nasopharyngeal carcinoma and breast cancer by using next-generation deep sequencing 13,14 . Moreover, THAP9-AS1 was delineated as an oncogenic factor in pancreatic ductal adenocarcinoma (PDAC) 15 and gastric cancer 16 . ...
Esophageal squamous cell carcinoma (ESCC) is one of the most common malignant tumors in the digestive system with a high incidence and poor prognosis. Long non-coding RNAs (LncRNA) have been reported to be closely associated with the occurrence and development of various human cancers. Data from GSE89102 shows an increase of THAP9-AS1 expression in ESCC. However, its functions and mechanisms underlying ESCC progression remain to be investigated. In this study, we found that THAP9-AS1 was overexpressed in ESCC tissues and cells. High THAP9-AS1 expression was positively correlated with tumor size, TNM stage, lymph node metastasis, and worse prognosis. Functionally, depletion of THAP9-AS1 suppressed cell proliferation, migration, and invasion, while enhanced apoptosis in vitro. Consistently, knockdown of THAP9-AS1 inhibited xenograft tumor growth in vivo. Mechanistically, THAP9-AS1 could serve as a competing endogenous RNA (ceRNA) for miR-133b, resulting in the upregulation of SOX4. Reciprocally, SOX4 bound to the promoter region of THAP9-AS1 to activate its transcription. Moreover, the anti-tumor property induced by THAP9-AS1 knockdown was significantly impaired due to miR-133b downregulation or SOX4 overexpression. Taken together, our study reveals a positive feedback loop of THAP9-AS1/miR-133b/SOX4 to facilitate ESCC progression, providing a potential molecular target to fight against ESCC.
... Genome wide association studies and NGS have revealed that the expression of 2192 lncRNAs change in the development and progression of NPC. This results in the upregulation of 62 genes that are controlled through these lncRNAs [51]. These include CD44 (Hyaluronan/CD44) and interleukin 1 receptor associated kinase 1 (IRAK1). ...
... These include CD44 (Hyaluronan/CD44) and interleukin 1 receptor associated kinase 1 (IRAK1). IRAK is involved in EBV infection while CD44 is involved in cancer progression [51]. LncRNAs that were downregulated in NPC include NR2F2 antisense RNA1 (NR2F21), lncRNA-family with sequence similarity 95 member C (FAM95C), and long intergenic nonprotein coding RNA 1106 (LIN-C01106). ...
... Those that were upregulated include lncRNA-CH507-513H4.6, lncRNA-THAP9 antisense RNA 1 (THAP9-AS1), lncRNACH507-513H4.3 and lncRNA-RP4-794H19.1 [51]. ...
It has been estimated that worldwide up to 10% of all human cancers are the result of viral infection, with 7.2% of all cancers in the developed world have a viral aetiology. In contrast, 22.9% of infections in the developing world are the result of viral infections. This number increases to 30% in Sub-Saharan Africa. The ability of viral infections to induce the transformation of normal cells into cancerous cells is well documented. These viruses are mainly Hepatitis B and C viruses, Epstein Barr virus, Human papillomavirus and Human Cytomegalovirus. They can induce the transformation of normal cells into cancer cells and this may be the underlying cause of carcinogenesis in many different types of cancer. These include liver cancer, lymphoma, nasopharyngeal cancer, cervical cancer, gastric cancer and even glioblastoma. Long non-coding RNAs (LncRNAs) can function by regulating the expression of their target genes by controlling the stability of the target mRNAs or by blocking translation of the target mRNA. They can control transcription by regulating the recruitment of transcription factors or chromatin modification complexes. Finally, lncRNAs can control the phosphorylation, acetylation, and ubiquitination of proteins at the post-translation level. Thus, altering protein localisation, function, folding, stability and ultimately expression. In addition to these functions, lncRNA also regulate alternate pre-mRNA splicing in ways that contribute to the formation of tumours. This mainly involves the interaction of lncRNAs with splicing factors, which alters their activity and function. The ability of lncRNAs to regulate the stability, expression and function of tumour suppressor proteins is important in the development and progression of cancers. LncRNAs also regulate viral replication and latency, leading to carcinogen-esis. These factors all make lncRNAs ideal targets for the development of biomarker arrays that can be based on secreted lncRNAs leading to the development of affordable non-invasive biomarker tests for the stage specific diagnosis of tumours. These lncRNAs can also serve as targets for the development of new anticancer drug treatments.
... 39 In our previous research, a new lncRNA RP11-624L4.1 was identified and was found to be highly expressed in NPC tissues using next-generation sequencing. 40 However, the NPC-causing roles and mechanisms of this novel lncRNA RP11-624L4.1 are unknown. Therefore, we examined the expression levels of RP11-624L4.1 in Chinese NPC tissue samples and further analyzed the clinicopathological significance and the prognosis of RP11-624L4.1 expression in a cohort of NPC patients. ...
... By RNA sequencing, we identified differentially expressed lncRNAs between seven inflammatory nasopharyngeal epithelium (NPE) tissues and seven NPC tissues, 40 and 2,192 lncRNAs were found to be differentially expressed. Among these, 204 lncRNAs were considered to be significantly downregulated, and 306 lncRNAs were considered to be significantly upregulated (R2-fold change, false discovery rate [FDR] < 0.05). ...
... Subsequently, first-strand cDNA was synthesized from 1 mg total RNA using the GoScript Reverse Transcription System (Promega, USA), followed by qPCR using the SYBR Green PCR master mix (Promega, USA) and a LightCycler 480 II System (Roche, USA). 40 Data were normalized to the expression level of b-actin and further normalized to the negative control. The relative expression of each target gene was calculated using the 2ÀDDCt method. ...
Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors in southern China and southeast Asia. Emerging evidence revealed that long noncoding RNAs (lncRNAs) might play important roles in the development and progression of many cancers, including NPC. The functions and mechanisms of the vast majority of lncRNAs involved in NPC remain unknown. In this study, a novel lncRNA RP11-624L4.1 was identified in NPC tissues using next-generation sequencing. In situ hybridization (ISH) was used to analyze the correlation between RP11-624L4.1 expression and the clinicopathological features or prognosis in NPC patients. RNA-Protein Interaction Prediction (RPISeq) predictions and RNA-binding protein immunoprecipitation (RIP) assays were used to identify RP11-624L4.1’s interactions with cyclin-dependent kinase 4 (CDK4). As a result, we found that RP11-624L4.1 is hyper-expressed in NPC tissues, which was associated with unfavorable prognosis and clinicopathological features in NPC. By knocking down and overexpressing RP11-624L4.1, we also found that it promotes the proliferation ability of NPC in vitro and in vivo through the CDK4/6-Cyclin D1-Rb-E2F1 pathway. Overexpression of CDK4 in knocking down RP11-624L4.1 cells can partially rescue NPC promotion, indicating its role in the RP11-624L4.1-CDK4/6-Cyclin D1-Rb-E2F1 pathway. Taken together, RP11-624L4.1 is required for NPC unfavorable prognosis and proliferation through the CDK4/6-Cyclin D1-Rb-E2F1 pathway, which may be a novel therapeutic target and prognostic in patients with NPC.
... On the contrary, LncRNA HOX transcript antisense intergenic RNA (HOTAIR) acts as an oncogene, whose high abundance in NPC cells and the patient tumor samples correlates with a poor prognosis [7,8]. With the advance of microarray and high-throughput RNA sequencing, a large number of lncRNAs have been identified in NPC tissues and cell lines [9]. However, the roles of these dysregulated lncRNAs in the pathogenesis of NPC remain poorly understood. ...
Abstract Nasopharyngeal carcinoma (NPC) is an epithelial cancer emerging from the lining of nasopharyngeal mucosa, with extremely frequent occurrence in east and southeast Asia. For the purpose of exploring roles of the dysregulated long non-coding RNA (lncRNA) in NPC, we identified a novel lncRNA LINC00669 with an apparent negative correlation to the overall survival from human NPC mRNA expression profiling databases. We further performed RNA pulldown coupled with mass spectrum to find out its target protein, and applied a series of in vitro and in vivo loss-and-gain-of function assays to investigate its oncogenic roles in NPC tumor development and progression. Our results demonstrated that LINC00669 competitively binds to the key JAK/STAT signaling pathway suppressor SOCS1, and insulates it from imposing ubiquitination modification on the pathway component of STAT1, which leads to its abnormal stabilization and activation. The activated STAT1 is then transferred into the nucleus and initiates the transcription of genes related to proliferation and invasion. In summary, our study reveals that the cytoplasmic resident lncRNA LINC00669 confers malignant properties on NPC cancer cells by facilitating a persistent activation of the JAK/STAT signaling pathway. Findings in the current study shed lights on prospects for treating NPC using strategies targeting the novel regulator of the JAK/STAT signaling.
