Identification of the Key Genes and Pathways in Esophageal Carcinoma

Su, Peng; Su, Wen Pang; Zhang, Yuefeng; Yong, Li; Xu, Yong; Zhu, Yao; Lv, Huilai; Zhang, Fan; Wang, Ming-Bo; Tian, Ziqiang

doi:10.1155/2016/2968106

Cited by 22 publications

(16 citation statements)

References 45 publications

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“…CDK4 was the node with the highest degree of interaction and was the most connected hub protein, interacting with 30 genes in the regulatory network. This result was consistent with that by Su et al ( 41 ), which also indicated that CDK4 was the most significantly upregulated gene by analyzing 5 mRNA expression datasets of EC tissues/cell lines from GEO. A recent study revealed that CDK4 had a negative association with EC-related gene 4, which has a tumor suppressor function in ESCC ( 42 ).…”

Section: Discussionsupporting

confidence: 92%

Identification of key genes and pathways for esophageal squamous cell carcinoma by bioinformatics analysis

Chen

Cai

et al. 2018

Exp Ther Med

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The aim of the present study was to identify the differentially expressed genes (DEGs) in esophageal squamous-cellcarcinoma (ESCC) and provide potential therapeutic targets. The microarray dataset GSE20347 was downloaded from the Gene Expression Omnibus (GEO) database, and included 17 tissue samples and 13 normal adjacent tissue samples from patients with ESCC. A total of 22,277 DEGs were identified. A heat map for the DEGs was constructed with the Morpheus online tool and the top 200 genes (100 upregulated and 100 downregulated) were selected for further bioinformatics analysis, including analysis of gene ontology (GO) terms, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways, protein-protein interaction networks and Spearman's correlation tests. The results of the GO analysis indicated that the upregulated DEGs were most significantly enriched in membrane-bounded vesicles in the cellular component (CC) category, but were not significantly enriched in any GO terms of the categories biological process (BP) or molecular function (MF); furthermore, the downregulated DEGs were most significantly enriched in regulation of DNA metabolic processes, nucleotide binding and chromosomes in the categories BP, MF and CC, respectively. The KEGG analysis indicated that the downregulated DEGs were enriched in the regulation of cell cycle pathways. The top 10 hub proteins in the protein-protein interaction network were cyclin-dependent kinase 4, budding uninhibited by benzimidazoles 1, cyclin B2, heat shock protein 90AA1, aurora kinase A, H2A histone family member Z, replication factor C subunit 4, and minichromosome maintenance complex component 2, −4 and −7. These proteins are mainly involved in regulating tumor progression. The genes in the four top modules were mainly implicated in regulating cell cycle pathways. Secreted Ly-6/uPAR-related protein (SLURP) was the hub gene, and SLURP and its interacting genes were most enriched in the chromosomal part in the CC category, organelle organization in the BP category and protein binding in the MF category, and were involved in pathways including DNA replication, cell cycle and P53 signaling. The expression of SLURP-1 in fifteen patients with esophageal carcinoma was detected using quantitative polymerase chain reaction analysis, and the results indicated that SLURP-1 expression was significantly decreased in the tumor samples relative to that in normal adjacent tissues. These results suggest that several hub proteins and the hub gene SLURP-1 may serve as potential therapeutic targets, and that gene dysfunction may be involved in the tumorigenesis of ESCC.

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Section: Discussionsupporting

confidence: 92%

Identification of key genes and pathways for esophageal squamous cell carcinoma by bioinformatics analysis

Chen

Cai

et al. 2018

Exp Ther Med

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“…Our previous study has identified key DEGs in ESCC by integrated analysis of five microarray datasets from GEO (19). With GEO database updated, we identified DEGs in ESCC by integrated analysis of ten microarray datasets with larger sample size in this study.…”

Section: Discussionmentioning

confidence: 98%

Identification of the key transcription factors in esophageal squamous cell carcinoma

Zhang¹,

Xu²,

Li³

et al. 2018

J. Thorac. Dis.

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Background: Esophageal cancer (EC) is a common human malignancy worldwide. Esophageal squamous cell carcinoma (ESCC) is the predominant subtype in China. The tumorigenesis mechanism in ESCC is unclear. The aim of this study was to identify key transcription factors (TFs) in ESCC and elucidate the mechanism of it. Methods: A total of ten published microarray datasets of ESCC was downloaded from the Gene Expression

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“…Clinical data showed that overexpression of CDKN3 indicated poor cancer prognosis13, 16. It had been documented that CDKN3 is upregulated in esophageal cancer17, but advanced research on the detailed biological function is still absent.…”

Section: Introductionmentioning

confidence: 99%

Cyclin-Dependent Kinase Inhibitor 3 Promoted Cell Proliferation by Driving Cell Cycle from G1 to S Phase in Esophageal Squamous Cell Carcinoma

Liu¹,

Min²,

Zhu³

et al. 2019

J. Cancer

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Background and aims . Cyclin-dependent kinase inhibitor 3 (CDKN3) has been found playing a varying role in carcinogenesis, but its biological function in esophageal squamous cell carcinoma (ESCC) is unclear. The aim of this study was to demonstrate the role of CDKN3 in ESCC. Materials and Methods: Real-time PCR and Western blot was performed in 15 pairs of ESCC tissues and adjacent normal esophageal tissues. Then cell proliferation ability, cloning ability, cell cycle status and migration and invasion ability were explored in CDKN3 overexpressed TE1 cell line and CDKN3 siRNA transfected TE1 and KYSE70 cell lines. Finally, cell cycle related proteins CyclinD1, CDK4, pAKT, P53, P21, and P27 were tested by Western blot. Results: mRNA level was higher in 11 ESCC tissues compared to adjacent normal tissues, and an increased protein expression was further detected in 8 of those 11 ESCC tissues. Functional assays showed that CDKN3 overexpression promoted ESCC cell proliferation, colony formation, migration and invasion, and facilitated G1/S transition. Opposite results were also got after transfected with CDKN3 siRNA. Cell cycle associated protein pAKT, CyclinD1, CDK4 and P27 were upregulated and P53, P21 and were downregulated under CDKN3 overexpression. All the protein levels were found changed in the opposite direction when CDKN3 expression was disturbed by siRNA. Conclusions : Our study suggested that CDKN3 acted as an oncogene in human ESCC and may accelerate the G1/S transition by affecting CyclinD-CDK4 complex via regulating pAKT-p53-p21 axis and p27 independent of AKT.

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Identification of the Key Genes and Pathways in Esophageal Carcinoma

Cited by 22 publications

References 45 publications

Identification of key genes and pathways for esophageal squamous cell carcinoma by bioinformatics analysis

Identification of key genes and pathways for esophageal squamous cell carcinoma by bioinformatics analysis

Identification of the key transcription factors in esophageal squamous cell carcinoma

Cyclin-Dependent Kinase Inhibitor 3 Promoted Cell Proliferation by Driving Cell Cycle from G1 to S Phase in Esophageal Squamous Cell Carcinoma

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