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Integrated analysis of a lncRNA?mRNA network reveals a potential mechanism underlying necrotizing enterocolitis.

ABSTRACT: Previous studies have shown that long non?coding RNAs (lncRNAs) serve important roles in necrotizing enterocolitis (NEC). However, the underlying mechanisms remain largely unknown. In order to examine the potential role of lncRNAs in NEC, the present study investigated lncRNA and mRNA expression profiles in NEC lesions and adjacent intestinal tissues using Next Generation Sequencing. A total of 4,202 differentially expressed lncRNAs (fold?change >2; P<0.05) and 7,860 differentially expressed mRNAs (fold?change >2; P<0.05) were identified. Moreover, 5 dysregulated lncRNAs and 5 mRNAs were randomly selected, and further assessed by reverse transcription?quantitative PCR in vitro. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses demonstrated that the differentially expressed lncRNAs were closely associated with NEC, and were enriched in 'inflammatory response', 'Toll?like receptor binding', 'PPAR signaling pathway', 'PI3K?Akt signaling pathway', 'transforming growth factor?? signaling pathway' and 'hypoxia?inducible factor 1 signaling pathway'. In addition, co?expression analysis demonstrated that these lncRNAs, including lncRNA ENST00000623580, lncRNA NONHSAT180418.1, lncRNA NONHSAT125636.2 and NONHSAT087855.2, may mediate the pathogenesis and development of NEC via lncRNA?mRNA network interactions. Therefore, the present study provided a novel insight into the role of lncRNAs in NEC.

SUBMITTER: Chen W

PROVIDER: S-EPMC7248486 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Integrated analysis of a lncRNA‑mRNA network reveals a potential mechanism underlying necrotizing enterocolitis.

Chen Wenjuan W Yan Xiangyun X Tian Tian T Yan Ru R Wang Xingyun X Yu Zhangbin Z Li Yingzheng Y Zhang Le L Han Shuping S

Molecular medicine reports 20200421 1

Previous studies have shown that long non‑coding RNAs (lncRNAs) serve important roles in necrotizing enterocolitis (NEC). However, the underlying mechanisms remain largely unknown. In order to examine the potential role of lncRNAs in NEC, the present study investigated lncRNA and mRNA expression profiles in NEC lesions and adjacent intestinal tissues using Next Generation Sequencing. A total of 4,202 differentially expressed lncRNAs (fold‑change >2; P<0.05) and 7,860 differentially expressed mRN ...[more]

PMID: 32319640

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Project description:Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are widely used for patients with EGFR-mutated lung cancer. Despite its initial therapeutic efficacy, most patients eventually develop drug resistance, which leads to a poor prognosis in lung cancer patients. Previous investigations have proved that non-coding RNAs including long non-coding RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs) contribute to drug resistance by various biological functions, whereas how they regulate EGFR-TKI resistance remains unclear. In this study, we examined gene expression using the microarray technology on gefitinib-resistant NSCLC cells to obtain differentially expressed (DE) lncRNAs and mRNAs. A total of 45 DE-lncRNAs associated with overall survival and 1799 target DE-mRNAs were employed to construct a core lncRNA-miRNA-mRNA network to illustrate underlying molecular mechanisms of how EGFR-TKI resistance occurs in NSCLC. We found that target DE-mRNAs were mainly enriched in pathways involved in EGFR-TKI resistance, especially the target DE-mRNAs regulated by LINC01128 were significantly enriched in the PI3K/Akt signaling pathway, where the synergy of these target DE-mRNAs may play a key role in EGFR-TKI resistance. In addition, downregulated LINC01128, acting as a specific miRNA sponge, decreases PTEN via sponging miR-25-3p. Furthermore, signaling reactions caused by the downregulation of PTEN would activate the PI3K/Akt signaling pathway, which may lead to EGFR-TKI resistance. In addition, a survival analysis indicated the low expression of LINC01128, and PTEN is closely related to poor prognosis in lung adenocarcinoma (LUAD). Therefore, the LINC01128/miR-25-3p/PTEN axis may promote EGFR-TKI resistance via the PI3K/Akt signaling pathway, which provides new insights into the underlying molecular mechanisms of drug resistance to EGFR-TKIs in NSCLC. In addition, our study sheds light on developing novel therapeutic approaches to overcome EGFR-TKI resistance in NSCLC.

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Integrated analysis of a lncRNA?mRNA network reveals a potential mechanism underlying necrotizing enterocolitis.

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Integrated analysis of a lncRNA‑mRNA network reveals a potential mechanism underlying necrotizing enterocolitis.

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