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- Relation of the Expression of Cyclooxygenase-2 in Colorectal Adenomas and Adenocarcinomas to Angiogenesis and Prognosis
- Yoon Dae Han, Young Ki Hong, Jung Gu Kang, Yoon Jung Choi, Chan Heun Park
- J Korean Soc Coloproctol. 2010;26(5):339-346. Published online October 31, 2010
- DOI: https://doi.org/10.3393/jksc.2010.26.5.339
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- 7 Citations
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Abstract
PDF Purpose Recent studies have shown that cyclooxygenase (COX)-2 may be involved in tumor growth, invasion and apoptosis in various carcinomas. Vascular endothelial growth factor (VEGF) has a potent angiogenic activity, and COX-2 promotes angiogenesis by modulating angiogenic factors, including VEGF. Endothelial growth factor receptor (EGFR) is considered as a factor of cell growth, maturation and cell death. The current study was designed to investigate the possible roles of COX-2 in colorectal tumor progression and angiogenesis.
Methods Fifty colorectal adenomas and forty adenocarcinomas were investigated by using immunohistochemical staining for COX-2, VEGF and EGFR. The correlations of COX-2, VEGF and EGFR with the grade of dysplasia, the size of the adenoma, and various clinicopathologic factors were studied.
Results The expressions of COX-2, VEGF and EGFR were each significantly correlated with carcinomatous transformation, and the expressions of COX-2 and VEGF were significantly correlated. COX-2 and EGFR showed correlations with adenomas rather than adenocarcinomas. However, no correlations of COX-2, VEGF and EGFR expression to other clinicopathologic factors, except tumor size in EGFR expression, were detected.
Conclusion These results suggest that COX-2 may play an important role in carcinogenesis through interaction with VEGF and EGFR in human colorectal cancer.
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Citations
Citations to this article as recorded by
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Journal of the Korean Society of Food Science and Nutrition.2023; 52(1): 8. CrossRef - Ocoxin® oral solution slows down tumor growth in an experimental model of colorectal cancer metastasis to the liver in Balb/c mice
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Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics.2013; 20(8): 369. CrossRef - Effects of Resveratrol on Migration and Proliferation in HT-29 Colon Cancer Cells
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KSBB Journal.2012; 27(5): 289. CrossRef - Anti-Proliferative Effects of Selenium in HT-29 Colon Cancer Cells via Inhibition of Akt
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Journal of Life Science.2012; 22(1): 55. CrossRef
- In Vitro Anticancer Effects of Unitein and Deep Seawater Salt Minerals on HT-29 Human Colon Carcinoma Cells
- Expression of Vascular Endothelial Growth Factor and Tumor Necrosis Factor-alpha in Angiogenesis Induced by Lipopolysaccharide and Thalidomide in CT26 Murine Colon Cancer of BALB/c Mouse.
- Choi, Dong Lak , Cho, Chang Ho , Jeong, Jin Sook , Hong, Sook Hee , Yoon, Ghil Suk
- J Korean Soc Coloproctol. 2004;20(3):125-132.
- 1,330 View
- 5 Download
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Abstract
PDF
- PURPOSE
The growth, progression, and metastasis of malignant neoplasms are influenced by the environment of the tumor and by proliferation of the tumor itself. Angiogenesis of a malignant neoplasm is a very important environmental factor of tumor growth and metastasis. Also, it is a prognostic factor for malignant neoplasms. The mechanism of angiogenesis, such as the effects of cytokines and angiogenesis-promoting factors, is incompletely understood.
METHODS
This study was designed to define the role of tumor necrosis factor-alpha (TNF-alpha) and the vascular endothelial growth factor (VEGF) in angiogenesis induced by lipopolysaccharide (LPS) and thalidomide (anticytokine drug) in CT26 murine colon cancer transplanted to BALB/c mice.
RESULTS
The tumor size in the LPS-treated group (n=3, 2.1+/-0.26 cm) was larger than it was in the LPS thalidomide-treated group (n=4, 1.95+/-0.19 cm) and in the control group (n=3, 1.6+/-0.20 cm) (P<0.05). The microvessel density determined by CD31 immunostaining was lowest for the control group and highest for the LPS- treated group, but the differences were not statistically significant. An immunohistochemical study showed that the expressions of TNF-alpha (P<0.01) and VEGF (P<0.05) were higher in the experimental groups than they were in the control group. Also, the LPS thalidomide-treated group had lower expressions of TNF-alpha (P<0.01) and VEGF (P<0.05) than the LPS-treated group. Western blots revealed that the TNF-alpha and the VEGF levels semiquantitatively increased from the control group to the LPS thalidomide-treated group to the LPS-treated group.
CONCLUSIONS
Our study revealed that low doses of LPS stimulated angiogenesis through increased expression of TNF-alpha and VEGF. Thalidomide decreased angiogenesis, probably through suppression of TNF-alpha with a decreased expression of VEGF. We conclude that TNF-alpha, suppressed by thalidomide, in the model of transplanted colon cancer may inhibit angiogenesis through coincident decrease in the expression of VEGF.
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