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Mol Med Rep. 2014 Oct;10(4):1800-12. doi: 10.3892/mmr.2014.2465. Epub 2014 Aug 7.

Functional analysis of the mRNA profile of neutrophil gelatinase‚ÄĎassociated lipocalin overexpression in esophageal squamous cell carcinoma using multiple bioinformatic tools.

Author information

1
Department of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou, Guangdong 515041, P.R. China.
2
Department of Pathology, Shantou Central Hospital, Affiliated Shantou Hospital of Sun Yat-sen University, Shantou, Guangdong 515041, P.R. China.
3
Department of Biochemistry and Molecular Biology, Guangdong Pharmaceutical University, Guangzhou Higher Education Mega Center, Guangzhou, Guangdong 510000, P.R. China.
4
Institute of Oncologic Pathology, Shantou University Medical College, Shantou, Guangdong 515041, P.R. China.

Abstract

Neutrophil gelatinase-associated lipocalin (NGAL) is a member of the lipocalin superfamily; dysregulated expression of NGAL has been observed in several benign and malignant diseases. In the present study, differentially expressed genes, in comparison with those of control cells, in the mRNA expression profile of EC109 esophageal squamous cell carcinoma (ESCC) cells following NGAL overexpression were analyzed by multiple bioinformatic tools for a comprehensive understanding. A total of 29 gene ontology (GO) terms associated with immune function, chromatin structure and gene transcription were identified among the differentially expressed genes (DEGs) in NGAL overexpressing cells. In addition to the detected GO categories, the results from the functional annotation chart revealed that the differentially expressed genes were also associated with 101 functional annotation category terms. A total of 59 subpathways associated locally with the differentially expressed genes were identified by subpathway analysis, a markedly greater total that detected by traditional pathway enrichment analysis only. Promoter analysis indicated that the potential transcription factors Snail, deltaEF1, Mycn, Arnt, MNB1A, PBF, E74A, Ubx, SPI1 and GATA2 were unique to the downregulated DEG promoters, while bZIP910, ZNF42 and SOX9 were unique for the upregulated DEG promoters. In conclusion, the understanding of the role of NGAL overexpression in ESCC has been improved through the present bioinformatic analysis.

PMID:
25109818
PMCID:
PMC4148386
DOI:
10.3892/mmr.2014.2465
[Indexed for MEDLINE]
Free PMC Article

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