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Updated: Sep 27, 2026

Evaluating the Angiogenetic Properties of Ovarian Cancer Stem-Like Cells using the Three-Dimensional Co-Culture System, NICO-1
07:59

Evaluating the Angiogenetic Properties of Ovarian Cancer Stem-Like Cells using the Three-Dimensional Co-Culture System, NICO-1

Published on: December 5, 2020

Cyclooxygenase-1 is overexpressed and promotes angiogenic growth factor production in ovarian cancer

Rajnish A Gupta1, Lovella V Tejada, Beverly J Tong

  • 1Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA.

Cancer Research
|March 5, 2003
PubMed

Insights

Cyclooxygenase-1 (COX-1) may drive ovarian cancer growth by promoting new blood vessel formation. Selective COX-1 inhibition, not COX-2, reduced tumor growth, suggesting COX-1 inhibitors may be more effective for ovarian cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Ovarian cancer is the leading cause of gynecological cancer mortality.
  • Cyclooxygenase-2 (COX-2) inhibitors have shown success in epithelial cancers, but their role in ovarian cancer is unknown.
  • Cytotoxic drugs used in ovarian cancer treatment can increase COX-2 expression.

Purpose of the Study:

  • To investigate the role of cyclooxygenase (COX) isoforms in ovarian cancer.
  • To determine if COX-1 or COX-2 is more critical in ovarian carcinoma development.
  • To evaluate the potential of COX inhibition as an adjuvant therapy for ovarian cancer.

Main Methods:

  • Analysis of COX-1 and COX-2 mRNA and protein expression in ovarian cancer tissues from patients not undergoing cytoreductive therapy.
  • Assessment of the effects of selective COX-1 and COX-2 inhibition on pro-angiogenic protein production.
  • Investigation of the role of prostaglandin E(2) in COX inhibition effects.

Main Results:

  • Most ovarian cancer specimens showed elevated levels of COX-1, not COX-2, mRNA and protein compared to normal tissue.
  • High COX-1 expression in tumors correlated with elevated pro-angiogenic proteins.
  • Selective inhibition of COX-1, but not COX-2, reduced vascular endothelial growth factor production, an effect reversible by prostaglandin E(2).

Conclusions:

  • COX-1, not COX-2, may contribute to ovarian cancer development by stimulating neovascularization.
  • Selective COX-1 or nonselective COX inhibitors may be more effective than COX-2 selective drugs as adjuvant therapy for ovarian cancer.

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