scholarly journals Integrated Analysis of Long Noncoding RNA and Coding RNA Expression in Esophageal Squamous Cell Carcinoma

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Wei Cao ◽  
Wei Wu ◽  
Fachun Shi ◽  
Xiaobing Chen ◽  
Lihua Wu ◽  
...  

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.

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Ling-zhao Meng ◽  
Ju-gao Fang ◽  
Jing-wu Sun ◽  
Fan Yang ◽  
Yong-xiang Wei

Objectives. This study aimed to identify aberrantly expressed long noncoding RNAs (lncRNAs) profile of sinonasal squamous cell carcinoma (SSCC) and explore their potential functions. Methods. We investigated lncRNA and mRNA expression in SSCC and paired adjacent noncancerous tissues obtained from 6 patients with microarrays. Gene ontology (GO) analysis and pathway analysis were utilized to investigate the gene function. Gene signal-network and lncRNA-mRNA network were depicted. Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized to validate 5 lncRNAs in a second set of paired SSCC and adjacent noncancerous tissues obtained from 22 additional patients. Results. We identified significantly differentially expressed lncRNAs (n=3146) and mRNAs (n=2208) in SSCC relative to noncancerous tissues. The GO annotation indicated that there are some core gene products that may be attributed to the progress of SSCC. The pathway analysis identified many pathways associated with cancer. The results of lncRNA-mRNA network and gene signal-network implied some core lncRNAs/mRNAs might play important roles in SSCC pathogenesis. The results of qRT-PCR showed that all of the 5 lncRNAs were differentially expressed and consistent with the microarray results. Conclusion. Our study is the first screening and analysis of lncRNAs expression profile in SSCC and may offer new insights into pathogenesis of this disease.


2019 ◽  
Vol 11 ◽  
pp. 175883591983895 ◽  
Author(s):  
Jian-Liang Chen ◽  
Zhi-Xiong Lin ◽  
Yun-Sheng Qin ◽  
Yu-Qi She ◽  
Yun Chen ◽  
...  

Background: Genome-wide sequencing investigations have identified numerous long noncoding RNAs (lncRNAs) among mammals, many of which exhibit aberrant expression in cancers, including esophageal squamous cell carcinoma (ESCC). Herein, this study elucidates the role and mechanism by which LINC01419 regulates the DNA methylation of glutathione S-transferase pi 1 (GSTP1) in relation to ESCC progression and the sensitivity of ESCC cells to 5-fluorouracil (5-FU). Methods: LINC01419 and GSTP1 levels were quantified among 38 paired ESCC and adjacent tissue samples collected from patients with ESCC. To ascertain the contributory role of LINC01419 in the progression of ESCC and identify the interaction between LINC01419 and GSTP1 promoter methylation, LINC01419 was overexpressed or silenced, and the DNA methyltransferase inhibitor 5-Aza-CdR was treated. Results: Data from the GEO database (GSE21362) and the Cancer Genome Atlas displayed elevated levels of LINC01419 and downregulated levels of GSTP1 in the ESCC tissues and cells. The silencing of LINC01419 led to decreased proliferation, increased apoptosis, and enhanced sensitivity to 5-FU in ESCC cells. Notably, LINC01419 could bind to the promoter region of the GSTP1 gene, resulting in elevated GSTP1 methylation and reduced GSTP1 levels via the recruitment of DNA methyltransferase among ESCC cells, whereby ESCC progression was stimulated accompanied by reduced ESCC cell sensitivity to 5-FU. GSTP1 demethylation by 5-Aza-CdR was observed to reverse the effects of LINC01419 overexpression in ESCC cells and the response to 5-FU. Conclusion: Highly expressed LINC01419 in ESCC promotes GSTP1 methylation, which ultimately acts to promote the event of ESCC and diminish the sensitivity of ESCC cells to 5-FU, highlighting a novel potential strategy to improve 5-FU-based chemotherapy in ESCC.


2021 ◽  
Vol 12 ◽  
Author(s):  
Yi Shen ◽  
Yi Shao ◽  
Chen Niu ◽  
Xiaoli Ruan ◽  
Zhaoping Zang ◽  
...  

BackgroundCircular RNAs (circRNAs) are described as endogenous non-coding RNAs that have been reported to play important roles in the development and progression of cancers. This study aimed to reveal the circRNA-related regulatory mechanism in esophageal squamous cell carcinoma (ESCC).MethodsA genome-wide circRNA microarray assay was performed to profile the expression of circRNAs in the blood of preoperative ESCC patients and healthy controls. A systematic method of data mining was performed to identify the differentially expressed miRNAs (DEmiRs) and differentially expressed genes (DEGs) based on the metaMA and RankProd analysis. Bioinformatics analyses and multiple tools were employed to construct the potential circRNA–miRNA–mRNA regulatory network.ResultsThirty-three differentially expressed circRNAs were identified in the ESCC blood, including 31 downregulated and two upregulated circRNAs in the blood of ESCC patients compared with the healthy controls. Twenty-three DEmiRs and 2,220 DEGs were obtained by the integration of microarray datasets. An ESCC-associated circRNA–miRNA–mRNA network was constructed based on 31 circRNAs, 3 DEmiRs, and 190 DEGs. Enrichment analyses indicated that the DEGs were associated with a series of biological processes and cancer-related pathways. The protein–protein interaction (PPI) network was generated by the 190 DEGs, with 10 hub genes verified in the network. Subsequently, a sub-network was established for ESCC, which included 29 circRNAs, 2 miRNAs, and 10 hub genes.ConclusionOur study provided a novel clue to help understand the circRNA–miRNA–mRNA regulatory mechanism, highlighting the potential roles of circRNAs in the pathogenesis and development of ESCC.


Tumor Biology ◽  
2014 ◽  
Vol 35 (8) ◽  
pp. 7743-7754 ◽  
Author(s):  
Hai-Wei Xie ◽  
Qing-Quan Wu ◽  
Bin Zhu ◽  
Fang-Jun Chen ◽  
Lv Ji ◽  
...  

2017 ◽  
Vol 32 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Hongfen Liu ◽  
Qiang Zhen ◽  
Yakun Fan

Background Recent studies have shown that long noncoding RNA (IncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) was involved in the progression of tumors. However, the role of GHET1 in esophageal squamous cell carcinoma (ESCC) remains unclear. Methods The expression of IncRNA GHET1 was examined in 55 paired ESCC tissues and adjacent nontumor tissues. Molecular and cellular techniques were used to explore the role of GHET1 on ESCC cells. Results Our data showed that GHET1 expression was significantly increased in ESCC tissues and cell lines. High GHET1 expression in ESCC tissues was significantly associated with poor differentiation, advanced tumor nodes metastasis stage, and lymph node metastasis. GHET1 showed high sensitivity and specificity for diagnosing ESCC. Our data from in vitro assays showed that GHET1 inhibition suppressed ESCC cells proliferation, migration, and invasion, and induced cells apoptosis. Furthermore, western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin. Conclusions Our study indicates that GHET1 acts as an oncogene in ESCC and may represent a novel therapeutic target for the treatment of ESCC patients.


Oncotarget ◽  
2016 ◽  
Vol 7 (51) ◽  
pp. 84480-84485 ◽  
Author(s):  
Xuemei Chen ◽  
Hongyu Han ◽  
Yuqi Li ◽  
Qiongxia Zhang ◽  
Kailan Mo ◽  
...  

2013 ◽  
Author(s):  
Yukie Sato-Kuwabara ◽  
Fabio Albuquerque Marchi ◽  
Clóvis Klock ◽  
Cristovam Scapulatempo ◽  
Felipe Coimbra ◽  
...  

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