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Bombesin/gastrin-releasing peptide antagonists RC-3095 and RC-3940-II inhibit tumor growth and decrease the levels

M Koppán1, G Halmos, J M Arencibia

  • 1Endocrine, Polypeptide and Cancer Institute, Veterans Affairs Medical Center, New Orleans, Louisiana 70146, USA.

Cancer
|October 8, 1998
PubMed
Abstract

Insights

Bombesin/gastrin-releasing peptide (BN/GRP) antagonists RC-3095 and RC-3940-II significantly reduced small cell lung carcinoma (SCLC) tumor growth. These BN/GRP antagonists also decreased epidermal growth factor receptor (EGF-R) levels and mRNA expression in SCLC tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Bombesin/gastrin-releasing peptide (BN/GRP) antagonists are developed to inhibit tumor growth in cancers like small cell lung carcinoma (SCLC) by blocking autocrine stimulatory effects.
  • The precise mechanism of action for BN/GRP antagonists, particularly concerning intracellular events and receptor modulation, remains incompletely understood.

Purpose of the Study:

  • To investigate the effects of synthetic BN/GRP antagonists, RC-3095 and RC-3940-II, on tumor growth in H-69 SCLC models.
  • To examine the impact of these antagonists on the expression of epidermal growth factor receptors (EGF-R) within SCLC tumors.

Main Methods:

  • Athymic nude mice xenografted with H-69 SCLC were treated subcutaneously for 5 weeks with BN/GRP antagonists RC-3095 and RC-3940-II.
  • Tumor volume, burden, and receptor expression levels (BN/GRP and EGF-R) were quantified.
  • Reverse transcriptase-polymerase chain reaction and Southern blot analyses were used to assess EGF-R mRNA levels.

Main Results:

  • Both RC-3095 and RC-3940-II significantly reduced H-69 SCLC tumor volume and burden.
  • Treatment with BN/GRP antagonists led to a significant decrease in the concentration of BN/GRP receptors and EGF-R.
  • A marked reduction in EGF-R mRNA levels was observed in tumors treated with RC-3095 and RC-3940-II.

Conclusions:

  • BN/GRP antagonists RC-3095 and RC-3940-II effectively inhibit the growth of H-69 SCLC.
  • The anti-tumor effect of these BN/GRP antagonists is associated with a significant downregulation of EGF-R expression at both protein and mRNA levels.

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