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Nuclear thioredoxin-1 is required to suppress cisplatin-mediated apoptosis of MCF-7 cells

Xiao-Ping Chen1, Shou Liu, Wen-Xin Tang

  • 1Key Laboratory of Molecular Biophysics of the Ministry of Education, College of Life Science and Technology, Huazhong University of Technology, Wuhan, 430074, China.

Biochemical and Biophysical Research Communications
|July 27, 2007
PubMed

Insights

Nuclear thioredoxin-1 (Trx-1) protects breast cancer cells from cisplatin-induced apoptosis. Increased nuclear Trx-1 is linked to cisplatin resistance, likely by upregulating the p53 gene.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Thioredoxin-1 (Trx-1) levels influence sensitivity to cisplatin.
  • Subcellular localization of Trx-1 is critical for its function.
  • The role of nuclear Trx-1 in breast cancer cell response to cisplatin is not fully understood.

Purpose of the Study:

  • To investigate the association between nuclear Trx-1 and cisplatin-mediated apoptosis in MCF-7 breast cancer cells.
  • To determine if nuclear Trx-1 contributes to cisplatin resistance.

Main Methods:

  • MCF-7 cells were transfected with Trx-1 cDNA.
  • Total and nuclear Trx-1 levels were assessed.
  • Cisplatin-induced apoptosis was measured.
  • mRNA levels of p53 were analyzed.

Main Results:

  • Increased total Trx-1 without altered nuclear Trx-1 did not affect cisplatin-induced apoptosis.
  • Elevated nuclear Trx-1, independent of total Trx-1, protected cells from cisplatin-induced apoptosis.
  • High nuclear Trx-1 correlated with cisplatin resistance in resistant cell lines.
  • Nuclear Trx-1 levels were closely correlated with p53 mRNA levels.

Conclusions:

  • Nuclear Trx-1 plays a crucial role in resisting cisplatin-induced apoptosis in MCF-7 cells.
  • Nuclear Trx-1 likely confers cisplatin resistance by upregulating the anti-apoptotic gene p53.

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