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Cell adhesion to fibronectin induces mitomycin C resistance in bladder cancer cells

Chun-Wu Pan1, Zhou-Jun Shen, Ting-Ting Wu

  • 1Department of Urology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

BJU International
|July 24, 2009
PubMed
Abstract

Insights

Fibronectin adhesion protects human bladder cancer cells from chemotherapy by activating the PI3-K/Akt pathway. This resistance involves inhibiting apoptosis pathways and regulating cell cycle progression.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Cell adhesion molecules like fibronectin play roles in cancer progression.
  • Drug resistance remains a significant challenge in bladder cancer treatment.

Purpose of the Study:

  • To determine if fibronectin adhesion confers drug resistance in human bladder cancer cells.
  • To elucidate the survival signaling pathway involved in fibronectin-mediated chemotherapy resistance.

Main Methods:

  • T24 bladder cancer cells were treated with mitomycin C (MMC) and fibronectin.
  • Apoptosis, cell cycle, and key protein expressions (PI3-K, Akt, GSK-3beta, cyclin D1) were analyzed.
  • Involvement of caspase and AIF pathways was assessed.

Main Results:

  • Fibronectin adhesion significantly reduced MMC-induced apoptosis in T24 cells.
  • Resistance was mediated by inhibiting caspase-9 and AIF pathways, not caspase-8.
  • Fibronectin stabilized cyclin D1 by inactivating GSK-3beta, preventing G0/G1 arrest.

Conclusions:

  • Fibronectin-mediated PI3-K/Akt activation confers resistance to mitomycin C in bladder cancer cells.
  • This protection involves suppressing caspase-9/AIF apoptosis and regulating GSK-3beta/cyclin D1 for cell cycle progression.

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