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pmid:36759514

Identification of potential biomarkers in Barrett's esophagus derived esophageal adenocarcinoma.

Nan Yi · Hailiang Zhao · Juan He · Xike Xie · Liexin Liang · Guowen Zuo · Mingyue Xiong · Yunxiao Liang · Tingzhuang Yi

Scientific reports · 2023 doi:10.1038/s41598-022-17107-0

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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title
Identification of potential biomarkers in Barrett's esophagus derived esophageal adenocarcinoma.
doi
10.1038/s41598-022-17107-0
pmid
36759514
authors array · 9 items
[0]
Nan Yi
[1]
Hailiang Zhao
[2]
Juan He
[3]
Xike Xie
[4]
Liexin Liang
[5]
Guowen Zuo
[6]
Mingyue Xiong
[7]
Yunxiao Liang
[8]
Tingzhuang Yi
journal
Scientific reports
year
2023
abstract
Almost 50% of esophageal adenocarcinoma (EAC) patients progressed from Barrett's esophagus (BE). EAC is often diagnosed at late stages and is related to dismal prognosis. However, there are still no effective methods for stratification and therapy in BE and EAC. Two public datasets (GSE26886 and GSE37200) were analyzed to identify differentially expressed genes (DEGs) between BE and EAC. Then, a series of bioinformatics analyses were performed to explore potential biomarkers associated with BE-EAC. 27 up- and 104 down-regulated genes were observed between GSE26886 and GSE37200. The GO and KEGG enrichment analysis indicated that the DEGs were highly involved in tumorigenesis. Subsequently, Weighted Gene Co-Expression Network Analysis (WGCNA) were performed to explore the potential genes related to BE-EAC, which were validated in The Cancer Genome Atlas (TCGA) database, and 5 up-regulated genes (MYO1A, ACE2, COL1A1, LGALS4, and ADRA2A) and 3 down-regulated genes (AADAC, RAB27A, and P2RY14) were found in EAC. Meanwhile, ADRA2A and AADAC could contribute to EAC pathogenesis and progression. MYO1A, ACE2, COL1A1, LGALS4, ADRA2A, AADAC, RAB27A, and P2RY14 could be potential novel diagnostic and prognostic biomarkers in BE-EAC.
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Considering that GSE26886 had larger sample size of EAC, it was used to detect modules highly correlated with EAC, and WGCNA was performed using R package “WGCNA”16 and carried out on all genes.
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sections[5] "Weighted gene co-expression network analysis (WGCNA)" paragraph 2
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Considering that GSE26886 had larger sample size of EAC, it was used to detect modules highly correlated with EAC, and WGCNA was performed using R package “WGCNA”16 and carried out on all genes.
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Publicly available datasets were analyzed in this study. This data can be found here: GEO data base, accession number: GSE26886 and GSE37200.
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The intersection of WGCNA trait-expression-related genes with DEGs yielded 27 genes for further analysis.
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sections[11] "Identification of key modules by WGCNA" paragraph 3
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In the module-trait analysis, we intersected the trait-related genes in grey module highly associated with EAC and 131 DEGs generated from expression difference analysis, and finally extracted 27 trait-expression-related genes for the following analysis (Fig. 3F, Tables S1 and S2).
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However, there are still no effective methods for stratification and therapy in BE and EAC. Two public datasets (GSE26886 and GSE37200) were analyzed to identify differentially expressed genes (DEGs) between BE and EAC. Then, a series of bioinformatics analyses were performed to explore potential biomarkers associated with BE-EAC. 27 up- and 104 down-regulated genes were observed between GSE26886 and GSE37200. The GO and KEGG enrichment analysis indicated that the DEGs were highly involved in tumorigenesis. Subsequently, Weighted Gene Co-Expression Network Analysis (WGCNA) were performed to explore the potential genes related to BE-EAC, which were validated in The Cancer Genome Atlas (TCGA) database, and 5 up-regulated genes (MYO1A, ACE2, COL1A1, LGALS4, and ADRA2A) and 3 down-regulated genes (AADAC, RAB27A, and P2RY14) were found in EAC. Meanwhile, ADRA2A and AADAC could contribute to EAC pathogenesis and progression. 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