Thalidomide down-regulates the expression of VEGF and bFGF in cisplatin-resistant human lung carcinoma cells

Xiping Li1, Xuyi Liu, Jie Wang

  • 1Mary Babb Randolph Cancer Center, Department of Microbiology, Immunology and Cell Biology, West Virginia University Robert C. Byrd Health Sciences Center, Morgantown, WV 26506, USA.

Anticancer Research
|August 5, 2003
PubMed

Insights

Thalidomide effectively suppresses vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in cisplatin-resistant lung cancer cells. This finding supports thalidomide

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Anti-angiogenic therapy is a key strategy in cancer treatment.
  • Thalidomide is known to inhibit angiogenesis and overcome drug resistance.
  • Its effect on angiogenic factors in cisplatin-resistant tumors remains unclear.

Purpose of the Study:

  • To investigate the impact of thalidomide on angiogenic growth factor expression in cisplatin-resistant lung cancer cells.
  • To evaluate thalidomide's potential in overcoming cisplatin resistance in lung carcinoma.

Main Methods:

  • Treatment of cisplatin-resistant human A549DDP lung carcinoma cells with thalidomide.
  • Analysis of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) mRNA levels using RT-PCR.
  • Quantification of VEGF and bFGF protein levels via dose- and time-dependent assays.

Main Results:

  • Thalidomide significantly decreased both mRNA and protein levels of VEGF and bFGF in A549DDP cells.
  • Suppression of growth factors occurred in a dose- and time-dependent manner.
  • Therapeutic concentrations of thalidomide (0.6-6 µg/ml) were effective.

Conclusions:

  • Thalidomide demonstrates potent suppression of key angiogenic factors in cisplatin-resistant lung cancer.
  • These findings suggest thalidomide's therapeutic potential for cisplatin-resistant lung cancer.
  • Further research into thalidomide's application in other resistant tumors is warranted.

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