[Expression and significance of FGFR2IIIc in chemoresistant bladder cancer cells]

Yule Chen1, Linlin Zhang2, Kaijie Wu2

  • 1Department of Urology, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an 710061, China.

Abstract

Insights

Fibroblast growth factor receptor-2 (FGFR2) splice variant FGFR2IIIc promotes mesenchymal-epithelial transition (MET) in doxorubicin-resistant bladder cancer cells. This process may contribute to the development of metastatic lesions in chemoresistant bladder cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Context:

  • Bladder cancer exhibits resistance to doxorubicin chemotherapy.
  • Chemotherapy resistance is often associated with cellular changes like the epithelial-mesenchymal transition (EMT).
  • Fibroblast growth factor receptor 2 (FGFR2) is implicated in various cellular processes, including cancer progression.

Purpose:

  • To investigate the role of the FGFR2 splice variant FGFR2IIIc in regulating mesenchymal-epithelial transition (MET) in doxorubicin-resistant bladder cancer cells.
  • To determine the expression levels of FGFR2IIIc and associated proteins in chemoresistant cells.
  • To assess the impact of FGFR2IIIc on cellular migration.

Summary:

  • Doxorubicin-resistant bladder cancer cells (253J/DOX) were generated and characterized.
  • Increased expression of P-glycoprotein and FGFR2IIIc was observed in resistant cells.
  • Resistant cells showed upregulation of E-cadherin, downregulation of vimentin, and reduced migration, indicating MET.

Impact:

  • FGFR2IIIc-induced MET in chemoresistant bladder cancer cells may be a key factor in the formation of metastatic lesions.
  • Understanding this mechanism could lead to novel therapeutic strategies for overcoming chemoresistance and preventing metastasis in bladder cancer.
  • This research highlights the potential of targeting FGFR2IIIc to manage advanced or metastatic bladder cancer.

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