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Updated: Jul 27, 2026

The Establishment of a Lung Colonization Assay for Circulating Tumor Cell Visualization in Lung Tissues
Published on: June 16, 2018
Host cyclooxygenase-2 modulates carcinoma growth
C S Williams1, M Tsujii, J Reese
1Department of Medicine, The Vanderbilt-Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2279, USA.
Cyclooxygenase-2 (COX-2) promotes tumor growth by enhancing vascularization. Inhibiting COX-2 in mice significantly reduced tumor size and blood vessel formation, highlighting its role in cancer progression.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cyclooxygenase-2 (COX-2; Ptgs2) is implicated as a tumor promoter in colorectal cancer models.
- The exact role of host-derived COX-1 and COX-2 in carcinogenesis requires further elucidation.
Purpose of the Study:
- To investigate the contribution of host-derived cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) in tumor growth.
- To assess the impact of COX-2 inhibition on tumor vascularization and proangiogenic factor production.
Main Methods:
- Utilized genetic approaches with COX-2 knockout (COX-2(-/-)) and wild-type mice, alongside pharmacological inhibition of COX-2.
- Implanted Lewis lung carcinoma (LLC) cells in C57BL/6 mice to model tumor growth.
- Assessed tumor vascular density and vascular endothelial growth factor (VEGF) production in mouse fibroblasts.
Main Results:
- Tumor growth was significantly attenuated in COX-2(-/-) mice compared to wild-type and COX-1(-/-) mice.
- Pharmacological inhibition of COX-2 in wild-type mice also reduced tumor growth.
- COX-2 deficiency in mouse fibroblasts led to a 94% reduction in VEGF production; COX-2 inhibition reduced VEGF by 92%.
Conclusions:
- Host-derived COX-2 plays a critical role in promoting tumor growth, independent of COX-1.
- COX-2 inhibition effectively reduces tumor growth and vascular density, likely by suppressing VEGF production in stromal fibroblasts.
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