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pmid:38560098

Bioinformatics analysis and validation of genes related to paclitaxel's anti-breast cancer effect through immunogenic cell death.

Qianmei Yang · Guimei Yang · Yi Wu · Lun Zhang · Zhuoyang Song · Dan Yang

Heliyon · 2024 doi:10.1016/j.heliyon.2024.e28409

Paper

complete

Experiment

complete

Data

partial

Analysis

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Execution

absent

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title
Bioinformatics analysis and validation of genes related to paclitaxel's anti-breast cancer effect through immunogenic cell death.
doi
10.1016/j.heliyon.2024.e28409
pmid
38560098
authors array · 6 items
[0]
Qianmei Yang
[1]
Guimei Yang
[2]
Yi Wu
[3]
Lun Zhang
[4]
Zhuoyang Song
[5]
Dan Yang
journal
Heliyon
year
2024
abstract
Research indicated that Paclitaxel (PTX) can induce immunogenic cell death (ICD) through immunogenic modulation. However, the combination of PTX and ICD has not been extensively studied in breast cancer (BRCA). The TCGA-BRCA and GSE20685 datasets were enrolled in this study. Samples from the TCGA-BRCA dataset were consistently clustered based on selected immunogenic cell death-related genes (ICD-RGs). Next, candidate genes were obtained by overlapping differentially expressed genes (DEGs) between BRCA and normal groups, intersecting genes common to DEGs between cluster1 and cluster2 and hub module genes, and target genes of PTX from five databases. The univariate Cox algorithm and the least absolute shrinkage and selection operator (LASSO) were performed to obtain biomarkers and build a risk model. Following observing the immune microenvironment in differential risk subgroups, single-gene gene set enrichment analysis (GSEA) was carried out in all biomarkers. Finally, the expression of biomarkers was analyzed. Enrichment analysis showed that 626 intersecting genes were linked with inflammatory response. Further five biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified and a risk model was built. The model's performance was validated using GSE20685 dataset. Furthermore, the biomarkers were enriched with adaptive immune response. Lastly, the experimental results indicated that the alterations in IL18, SH2D2A, and CHI3L1 expression after treatment matched those in the public database. In this study, Five PTX-ICD-related biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified to aid in predicting BRCA treatment outcomes.
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DEGs between the BRCA and normal were selected the edgeR package (v 3.36.0) [24] according to adjusted P < 0.05 and |log2FC| > 0.5 where the generalized linear model (GLM) and the ‘glmLRT’ function were conducted to flexibly adjust the sample design matrix to adapt to the unbalanced sample size between the BRCA (1072) and normal samples (99) [25].
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sections[4] "Screening for differentially expressed genes (DEGs) and identify subtypes" paragraph 2
quote
DEGs between the BRCA and normal were selected the edgeR package (v 3.36.0) [24] according to adjusted P < 0.05 and |log2FC| > 0.5 where the generalized linear model (GLM) and the ‘glmLRT’ function were conducted to flexibly adjust the sample design matrix to adapt to the unbalanced sample size between the BRCA (1072) and normal samples (99) [25].
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The datasets utilized and assessed in this study can be accessed from the UCSC Xene database (https://xenabrowser.net) and the GEO database (https://www.ncbi.nlm.nih.gov/gds) under the identifier [GSE20685].
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The datasets utilized and assessed in this study can be accessed from the UCSC Xene database (https://xenabrowser.net) and the GEO database (https://www.ncbi.nlm.nih.gov/gds) under the identifier [GSE20685].
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Five PTX-ICD-related biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified to aid in predicting BRCA treatment outcomes.
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Further five biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified and a risk model was built.
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Five PTX-ICD-related biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified to aid in predicting BRCA treatment outcomes.
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DEGs between the BRCA and normal were selected the edgeR package (v 3.36.0) [24] according to adjusted P < 0.05 and |log2FC| > 0.5 where the generalized linear model (GLM) and the ‘glmLRT’ function were conducted to flexibly adjust the sample design matrix to adapt to the unbalanced sample size between the BRCA (1072) and normal samples (99) [25].
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DEGs between the BRCA and normal were selected the edgeR package (v 3.36.0) [24] according to adjusted P < 0.05 and |log2FC| > 0.5 where the generalized linear model (GLM) and the ‘glmLRT’ function were conducted to flexibly adjust the sample design matrix to adapt to the unbalanced sample size between the BRCA (1072) and normal samples (99) [25].
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Complete file
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The TCGA-BRCA and GSE20685 datasets were enrolled in this study. Samples from the TCGA-BRCA dataset were consistently clustered based on selected immunogenic cell death-related genes (ICD-RGs). Next, candidate genes were obtained by overlapping differentially expressed genes (DEGs) between BRCA and normal groups, intersecting genes common to DEGs between cluster1 and cluster2 and hub module genes, and target genes of PTX from five databases. The univariate Cox algorithm and the least absolute shrinkage and selection operator (LASSO) were performed to obtain biomarkers and build a risk model. Following observing the immune microenvironment in differential risk subgroups, single-gene gene set enrichment analysis (GSEA) was carried out in all biomarkers. Finally, the expression of biomarkers was analyzed. Enrichment analysis showed that 626 intersecting genes were linked with inflammatory response. Further five biomarkers (CHI3L1, IL18, PAPLN, SH2D2A, and UBE2L6) were identified and a risk model was built. The model's performance was validated using GSE20685 dataset. Furthermore, the biomarkers were enriched with adaptive immune response. Lastly, the experimental results indicated that the alterations in IL18, SH2D2A, and CHI3L1 expression after treatment matched those in the public database. 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