BackgroundLong non-coding RNAs (lncRNAs) are pervasively transcribed in the genome. They have important regulatory functions in chromatin remodeling and gene expression. Dysregulated lncRNAs have been studied in cancers, but their role in esophageal squamous cell carcinoma (ESCC) remains largely unknown. We have conducted lncRNA expression screening and a genome-wide analysis of lncRNA and coding gene expression on primary tumor and adjacent normal tissue from four ESCC patients, tend to understand the functionality of lncRNAs in carcinogenesis of esopheagus in combination with experimental and bioinformatics approach.MethodsLncRNA array was used for coding and non-coding RNA expression. R program and Bioconductor packages (limma and RedeR) were used for differential expression and co-expression network analysis, followed by independent confirmation and functional studies of inferred onco-lncRNA ESCCAL-1 using quantitative real time polymerase chain reaction, small interfering RNA-mediated knockdown, apoptosis and invasion assays in vitro.ResultsThe global coding and lncRNA gene expression pattern is able to distinguish ESCC from adjacent normal tissue. The co-expression network from differentially expressed coding and lncRNA genes in ESCC was constructed, and the lncRNA function may be inferred from the co-expression network. LncRNA ESCCAL-1 is such an example as a predicted novel onco-lncRNA, and it is overexpressed in 65% of an independent ESCC patient cohort (n = 26). More over, knockdown of ESCCAL-1 expression increases esophageal cancer cell apoptosis and reduces the invasion in vitro.ConclusionOur study uncovered the landscape of ESCC-associated lncRNAs. The systematic analysis of coding and lncRNAs co-expression network increases our understanding of lncRNAs in biological network. ESCCAL-1 is a novel putative onco-lncRNA in esophageal cancer development.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1179-z) contains supplementary material, which is available to authorized users.

Tumorigenesis is a complex dynamic biological process that includes multiple steps of genetic and epigenetic alterations, aberrant expression of noncoding RNA, and changes in the expression profiles of coding genes. We call the collection of those perturbations in genome space the “cancer initiatome.” Long noncoding RNAs (lncRNAs) are pervasively transcribed in the genome and they have key regulatory functions in chromatin remodeling and gene expression. Spatiotemporal variation in the expression of lncRNAs has been observed in development and disease states, including cancer. A few dysregulated lncRNAs have been studied in cancers, but the role of lncRNAs in the cancer initiatome remains largely unknown, especially in esophageal squamous cell carcinoma (ESCC). We conducted a genome-wide screen of the expression of lncRNAs and coding RNAs from ESCC and matched adjacent nonneoplastic normal tissues. We identified differentially expressed lncRNAs and coding RNAs in ESCC relative to their matched normal tissue counterparts and validated the result using polymerase chain reaction analysis. Furthermore, we identified differentially expressed lncRNAs that are co-located and co-expressed with differentially expressed coding RNAs in ESCC and the results point to a potential interaction between lncRNAs and neighboring coding genes that affect ether lipid metabolism, and the interaction may contribute to the development of ESCC. These data provide compelling evidence for a potential novel genomic biomarker of esophageal squamous cell cancer.

The study aimed to screen potential key genes, and their targeted miRNAs and transcription factors (TFs) that were related to diffuse large B-cell lymphoma (DLBCL), and explore potential therapeutic targets for the progression of DLBCL. Dataset GSE56315 extracted from human tonsils was downloaded from Gene Expression Omnibus. Limma package was used to identify differential expression genes (DEG) between DLBCL and normal human tonsils samples, and the function and pathway enrichment analyses were performed. Then, functional interaction (FI) networks analyses of DEGs were implemented, and modules were extracted. Additionally, DLBCL-related miRNAs were predicted based on miR2disease database. Thereafter, TF-target DEGs and miRNAs targeted genes were respectively obtained. Finally, the integrated network of TF-target-miRNA was constructed. A total of 4,495 DEGs were identified between DLBCL and NHT samples. Among them, 114 up-regulated DEGs were contained in 8 modules of FI network, while 189 down-regulated DEGs were contained in 12 sub-modules. In addition, most DEGs were enriched in the function of "DNA binding" and pathways of "chemokine signaling pathway", "phosphatidylinositol signaling system" and "RNA degradation". Moreover, 19 miRNAs related with DLBCL were downloaded from Mirwalk2. Furthermore, miRNAs of miR-21-5p, miR-155 and miR-17-5p, the TF of STAT1, and DEGs such as NUF2, CCR1, PIK3R1, SMC1A, FOXK1 and CNOT6L had high degrees in the integrated networks of TF-target-miRNA. DEGs like NUF2, CCR1, PIK3R1, SMC1A, FOXK1 and CNOT6L might be closely associated with the pathogenesis of DLBCL.