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Published on: March 18, 2014
Effect of ketoprofen in topical formulation on vascular endothelial growth factor expression and tumor growth in nude
Kenshi Sakayama1, Teruki Kidani, Tatsuhiko Miyazaki
1Department of Orthopaedic Surgery, School of Medicine, Ehime University, Shigenobu, Onsen-gun, 791-0295, Japan. kenshi@m.ehime-u.ac.jp
Abstract:
OST cells, a low metastatic cell line established from human osteosarcoma, were inoculated under the periosteum of the ossa cranii of nude mice. Four weeks later, tumors were percutaneously treated for an additional 4 weeks with a patch containing either placebo or ketoprofen (KP). In the placebo group, OST cells formed osteoid and invaded the cranial bone. Tumor mass weighed 3.54 g. Approximately 85% of cells within the tumor expressed proliferating cell nuclear antigen (PCNA), indicating that they were proliferating with a high mitotic activity. Many feeder vessels were located within the tumor. The majority of tumor cells expressed intensely vascular endothelial growth factor (VEGF). In the KP group, invasion of OST cells into the cranial bone was suppressed and the tumor mass was 47% of that of the placebo group. Approximately 65% of cells within the tumor were PCNA-negative, indicating that their growth was arrested. There were considerably fewer feeder vessels within the tumor in the KP group than in the placebo group. Only a small number of cells expressed VEGF. Based on these findings, we concluded that topical administration of KP to nude mice with osteosarcoma inhibited VEGF expression, reduced the development of feeder vessels for supply of nutrients and oxygen, and suppressed tumor growth.
Insights
Topical ketoprofen (KP) significantly suppressed osteosarcoma tumor growth in mice. KP inhibited vascular endothelial growth factor (VEGF) and reduced tumor vascularization, leading to reduced tumor mass and suppressed cell proliferation.
Area of Science:
- Oncology
- Pharmacology
- Biomedical Research
Background:
- Osteosarcoma is a primary bone malignancy.
- Developing effective therapeutic strategies for osteosarcoma remains a challenge.
- Low metastatic OST cells provide a model for studying tumor progression and treatment.
Purpose of the Study:
- To investigate the efficacy of topical ketoprofen (KP) in inhibiting osteosarcoma tumor growth.
- To elucidate the mechanisms underlying KP's anti-tumor effects, focusing on vascular endothelial growth factor (VEGF) and tumor vascularization.
Main Methods:
- Human osteosarcoma (OST) cells were inoculated into the cranial bone of nude mice.
- Tumors were treated with topical placebo or ketoprofen (KP) patches.
- Tumor growth, cell proliferation (PCNA), vascularity, and VEGF expression were assessed.
Main Results:
- Ketoprofen (KP) treatment significantly reduced tumor mass by 47% compared to placebo.
- KP suppressed tumor cell proliferation, with a decrease in PCNA-positive cells from 85% to 65%.
- KP inhibited VEGF expression and reduced the number of feeder vessels within the tumor.
Conclusions:
- Topical ketoprofen (KP) effectively suppresses osteosarcoma growth in a preclinical model.
- KP exerts its anti-tumor effects by inhibiting VEGF, reducing tumor vascularization, and arresting cell proliferation.
- These findings suggest potential for topical ketoprofen as an adjunctive therapy for osteosarcoma.
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