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Globally construct ceRNA regulation network based on comparison with SHEE and SHEEC cell lines (RNA-Seq)

ABSTRACT: Long non-coding RNAs (lncRNAs), new star ncRNA class of mRNA-like transcripts, play complicate and critical roles in regulating various key biological processes including chromatin modification, transcription and post-transcriptional processing. Remarkably, some lncRNAs serve as a miRNA “sponge” to inhibit mediation of the differentiation of miRNA target in post-transcriptional regulation. Here, we firstly constructed the putative ceRNA network by integrating lncRNAs, miRNAs and mRNAs expression in compared with SHEE and SHEEC cell lines based on the high-though RNA sequencing data and microarray data. Though the biology function analysis, the result showed that ceRNA network mainly participate in PI3K-Akt pathway and may play a modulating role in regulation of essential signal molecules including SYK, FGF11, IL7R, MET, LAMB3, PRS6KB1, ITGB6, ITGB4, ITGA2, ITGA6, EPHA2, SOS2, VEGFA, GRB2, KRAS, CCDN1 and TP53 in primary ESCC. These results could provide us more essential clues for the development of novel therapeutic strategies and efficient drugs target in primary ESCC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72273 | GEO | 2017/06/12

SECONDARY ACCESSION(S): PRJNA293566

REPOSITORIES: GEO

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Project description:Background: Esophageal squamous cell carcinoma (ESCC) is a common invasive malignancy worldwide with poor clinical outcomes. Increasing amount of long non-coding RNAs (lncRNAs) have been reported to be involved in cancer development. However, lncRNAs that are functional in ESCC and the underlying molecular mechanisms remain largely unknown. Methods: Transcriptomic analysis was performed to identify dysregulated lncRNAs in ESCC tissue samples. The high expression of LINC00680 in ESCC was validated by RT-qPCR, and the oncogenic functions of LINC00680 was investigated by cell proliferation, colony formation, migration and invasion assays in ESCC cells in vitro and xenografts derived from ESCC cells in mice. RNA-seq, competitive endogenous RNA (ceRNA) network analysis, and luciferase reporter assays were carried out to identify LINC00680 target genes and the microRNAs (miRNAs) bound to LINC00680. Antisense oligonucleotides (ASOs) were used for in vivo treatment. Results: Transcriptome profiling revealed that a large number of lncRNAs was dysregulated in ESCC tissues. Notably, LINC00680 was highly expressed, and upregulation of LINC00680 was associated with large tumor size, advanced tumor stage, and poor prognosis. Functionally, knockdown of LINC00680 restrained ESCC cell proliferation, colony formation, migration, and invasion in vitro and inhibited tumor growth in vivo. Mechanistically, LINC00680 was found to act as a ceRNA by sponging miR-423-5p to regulate PAK6 (p21-activated kinase 6) expression in ESCC cells. The cell viability and motility inhibition induced by LINC00680 knockdown was significantly reversed upon PAK6 restoration and miR-423-5p inhibition. Furthermore, ASO targeting LINC00680 substantially suppressed ESCC both in vitro and in vivo. Conclusions: An oncogenic lncRNA, LINC00680, was identified in ESCC, which functions as a ceRNA by sponging miR-423-5p to promote PAK6 expression and ESCC. LINC00680/miR-423-5p/PAK6 axis may serve as promising diagnostic and prognostic biomarkers and therapeutic targets for ESCC.

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Globally construct ceRNA regulation network based on comparison with SHEE and SHEEC cell lines (RNA-Seq)

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