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pmid:40699768

TNF Signaling Pathway Is the Key Pathway Regulated by Disitamab Vedotin in Bladder Cancer Cells.

Xingxing Tang · Jia Liu · Qiang Zhao · Yudong Cao · Xiao Yang · Peng Du · Yong Yang

Current issues in molecular biology · 2025 doi:10.3390/cimb47050369

Paper

complete

Experiment

partial

Data

partial

Analysis

complete

Execution

absent

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title
TNF Signaling Pathway Is the Key Pathway Regulated by Disitamab Vedotin in Bladder Cancer Cells.
doi
10.3390/cimb47050369
pmid
40699768
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[0]
Xingxing Tang
[1]
Jia Liu
[2]
Qiang Zhao
[3]
Yudong Cao
[4]
Xiao Yang
[5]
Peng Du
[6]
Yong Yang
journal
Current issues in molecular biology
year
2025
abstract
Disitamab Vedotin has shown good therapeutic efficacy against bladder cancer. Although its mechanism is clear, the regulation of gene expression in bladder cancer cells by Disitamab Vedotin is not fully understood. We searched the GEO database and identified the GSE237789 dataset, in which researchers treated the bladder cancer cell line SW780 with Disitamab Vedotin and performed high-throughput transcriptome sequencing. Compared with the control SW780 cells, the expression levels of the vast majority of genes (16,223/16,390, 98.98%) in Disitamab Vedotin-treated SW780 cells remained unchanged. Only one hundred fifty-nine genes (0.97%) were upregulated, and eight genes (0.05%) were downregulated. Enrichment analysis results showed that the related differentially expressed genes (DEGs) were mainly enriched in the TNF signaling pathway, NF-κB signaling pathway, and other pathways. Protein-protein interaction analysis revealed that 10 genes, TNF, IL1B, IL1A, CXCL8, CXCL1, CCL2, MMP9, ICAM1, CXCL10, and CCL20, had the highest connectivity, and all of these genes belong to the TNF signaling pathway. These results suggest that the TNF signaling pathway is the key pathway regulated by Disitamab Vedotin in bladder cancer cells, which may represent a stress response of bladder cancer cells to Disitamab Vedotin.
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We analyzed the DEGs between the RC48 group and the control group in the GSE237789 dataset using R (version 4.4.2) and the limma package (version 3.62.2).
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sections[4] "2.2. Identification of Differentially Expressed Genes (DEGs)" paragraph 2
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The TNF signaling pathway was identified as the key pathway regulated by Disitamab Vedotin in bladder cancer cells, with 10 hub genes having the highest connectivity in the PPI network.
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These results suggest that the TNF signaling pathway is the key pathway regulated by Disitamab Vedotin in bladder cancer cells, which may represent a stress response of bladder cancer cells to Disitamab Vedotin.
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sections[0] "Abstract" paragraph 1
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Protein–protein interaction analysis revealed that 10 genes, TNF, IL1B, IL1A, CXCL8, CXCL1, CCL2, MMP9, ICAM1, CXCL10, and CCL20, had the highest connectivity, and all of these genes belong to the TNF signaling pathway.
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itamab Vedotin and performed high-throughput transcriptome sequencing. Compared with the control SW780
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ch at Peking University. The 5637 cells were cultured in Dulbecco’s Modified Eagle Medium (DMEM) cont
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Complete file
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We searched the GEO database and identified the GSE237789 dataset, in which researchers treated the bladder cancer cell line SW780 with Disitamab Vedotin and performed high-throughput transcriptome sequencing. Compared with the control SW780 cells, the expression levels of the vast majority of genes (16,223/16,390, 98.98%) in Disitamab Vedotin-treated SW780 cells remained unchanged. Only one hundred fifty-nine genes (0.97%) were upregulated, and eight genes (0.05%) were downregulated. Enrichment analysis results showed that the related differentially expressed genes (DEGs) were mainly enriched in the TNF signaling pathway, NF-κB signaling pathway, and other pathways. Protein-protein interaction analysis revealed that 10 genes, TNF, IL1B, IL1A, CXCL8, CXCL1, CCL2, MMP9, ICAM1, CXCL10, and CCL20, had the highest connectivity, and all of these genes belong to the TNF signaling pathway. 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