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

Area of Science:

• Oncology
• Molecular Biology
• Genomics

Background:

• Disitamab Vedotin demonstrates therapeutic potential in bladder cancer.
• The precise gene expression regulatory mechanisms of Disitamab Vedotin in bladder cancer remain incompletely understood.

Purpose of the Study:

• To investigate the global gene expression changes in bladder cancer cells following Disitamab Vedotin treatment.
• To identify key signaling pathways modulated by Disitamab Vedotin.

Main Methods:

• Utilized the GSE237789 dataset from the GEO database.
• Performed high-throughput transcriptome sequencing on SW780 bladder cancer cells treated with Disitamab Vedotin.
• Conducted enrichment analysis and protein-protein interaction analysis on differentially expressed genes (DEGs).

Main Results:

• Disitamab Vedotin treatment resulted in minimal changes to overall gene expression (98.98% unchanged).
• Identified 159 upregulated and 8 downregulated genes.
• Enrichment analysis highlighted the Tumor Necrosis Factor (TNF) and Nuclear Factor-kappa B (NF-κB) signaling pathways.
• Top connected genes (TNF, IL1B, IL1A, CXCL8, CXCL1, CCL2, MMP9, ICAM1, CXCL10, CCL20) were all part of the TNF signaling pathway.

Conclusions:

• The Tumor Necrosis Factor (TNF) signaling pathway is significantly regulated by Disitamab Vedotin in bladder cancer cells.
• This pathway activation may represent a cellular stress response to Disitamab Vedotin treatment.
• Findings provide insights into the molecular mechanisms of Disitamab Vedotin in bladder cancer.