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

Xingxing Tang1, Jia Liu1, Qiang Zhao1

  • 1Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Urology, Peking University Cancer Hospital & Institute, No. 52 Fucheng Road, Haidian District, Beijing 100142, China.

Current Issues in Molecular Biology
|July 23, 2025
PubMed

Insights

Disitamab Vedotin treatment in bladder cancer cells primarily activates the Tumor Necrosis Factor (TNF) signaling pathway. This suggests a stress response mechanism in cancer cells, offering new therapeutic insights.

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.
Keywords:
NF-κB signaling pathwayRC48TNF signaling pathwaybladder cancerdisitamab vedotin

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