Inhibition of lung adenocarcinoma LA795 in mice by recombinant human endostatin

De-Ling Liu1, Jin-Xu Wen, Wan-Cheng Tong

  • 1Department of Respiratory Disease, Fuzhou General Hospital, Fuzhou 350025, China.

Di 1 Jun Yi Da Xue Xue Bao = Academic Journal of the First Medical College of PLA
|November 12, 2002
PubMed

Insights

Recombinant human endostatin significantly inhibited lung adenocarcinoma LA795 tumor growth and metastasis in mice. This treatment also extended the survival time of tumor-bearing mice.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Lung adenocarcinoma is a significant cause of cancer mortality.
  • Endostatin is a potent endogenous angiogenesis inhibitor.
  • Targeting tumor angiogenesis is a promising therapeutic strategy.

Purpose of the Study:

  • To investigate the efficacy of recombinant human endostatin in inhibiting tumor growth and metastasis.
  • To evaluate the impact of endostatin on the survival of mice bearing lung adenocarcinoma.

Main Methods:

  • Purification of recombinant human endostatin from endostatin-expressing pCX clones.
  • Subcutaneous inoculation of LA795 lung adenocarcinoma cells in T739 mice.
  • Administration of recombinant human endostatin (20 mg/kg daily) or PBS to randomized groups for 14 days.

Main Results:

  • Significantly reduced tumor size in the endostatin treatment group compared to controls (1642 mm3 vs 9194 mm3).
  • Markedly decreased lung weight and number of lung surface metastases in treated mice (8+/-2 vs 22+/-8).
  • Prolonged average survival time in the endostatin group (48 days vs 27 days).

Conclusions:

  • Recombinant human endostatin demonstrates potent anti-tumor and anti-metastatic effects.
  • Endostatin therapy significantly improves survival in a murine model of lung adenocarcinoma.
  • These findings support endostatin as a potential therapeutic agent for lung cancer.

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