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LIMD2 is a prognostic and predictive marker in patients with esophageal cancer based on a ceRNA network analysis

Xinyi Huang  Qinyan Chen  Lin Chen  Yuanmei Chen  Kunshou Zhu  Junqiang Chen  Yuanji Xu  
【摘要】:Background: Globally, esophageal cancer(ECA) is the seventh most common cancer and sixth most common cause of cancer-associated mortality. However, there are no reliable prognostic and predictive molecular markers for ECA; in addition, the pathogenesis of ECA are not fully elucidated.This study was to explore the potential prognostic and predictive markers of ECA, as well as investigate the mechanisms of ECA.Methods: The expressions of circular RNAs(circRNAs), microRNAs(miRNAs), and messenger RNAs(mRNAs) of ECA and control groups were obtained from the RNA-sequencing(RNA-seq) data of our hospital, the Gene Expression Omnibus(GEO) and The Cancer Genome Atlas(TCGA) datasets.Analyses of differentially-expressed genes, the circRNA-miRNA-mRNA competing endogenous RNA(ceRNA) network, and functional/pathway enrichment were conducted. The key targets in the ceRNA network that showed significant results in survival Cox regression analyses were selected. Furthermore,analyses of immune infiltration and autophagy genes related to the key targets were performed.Results: Seven circRNAs, 22 miRNAs, and 34 mRNAs were identified as vital genes in ECA; the nuclear factor-κ-gene binding(NF-κB) and phosphatidylinositol-3 kinase/protein kinase B(PI3 K-Akt)signaling were identified as the most enriched pathways. In addition, LIM domain containing 2(LIMD2) was an independent predictor of prognosis in ECA patients, and closely associated with immunity and autophagy. Moreover, quantitative reverse-transcription polymerase chain reaction(qRT-PCR) revealed significant upregulation of LIMD2 expression in ECA tissues.Conclusions: ECA may be closely correlated with NF-κB and PI3 K/Akt signaling. In addition, LIMD2 could be a potential prognostic and predictive marker of ECA. Our study may provide novel insights into the prognosis and treatment of ECA by its pathogenesis.

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