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Updated: Jan 26, 2026
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Published on: October 28, 2021
The effect of non-steroidal anti-inflammatory drugs on osteosarcoma cells
L M Zuckerman1, W L Frames, J G Elsissy
1Department of Orthopaedic Surgery, Loma Linda University Medical Center, Loma Linda, CA, USA. wframes@llu.edu.
Objective:
Osteosarcoma (OS), an aggressive malignancy, is the most common primary bone tumor in children. Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used to reduce pain and inflammation. NSAIDs have shown to be toxic to certain malignancies such as colorectal, breast, and pancreatic cancers, but are not well-studied in OS. The purpose of this study is to assess whether ketorolac induces apoptosis in OS cells, compare this to indomethacin, which has been shown to inhibit OS proliferation, and explore the underlying mechanism.
Materials And Methods:
A rat OS cell line (UMR-108) was exposed to various concentrations of ketorolac and indomethacin. Cell viability, cytotoxicity, apoptosis induction, DNA fragmentation and the expression of apoptosis-related markers were examined by MTT assay, colony formation assay, flow cytometry, agarose gel electrophoresis, and Western blot respectively.
Results:
The results indicated that ketorolac and indomethacin could induce apoptosis of rat OS cells in a dose- and time-dependent manner. Apoptosis was confirmed by cell morphology and annexin positivity. The molecular data showed that NSAIDs affected expression of Bcl-2, survivin, and Poly (ADP-ribose) polymerase-1 (PARP).
Conclusions:
These findings demonstrated that NSAIDs induced apoptosis in rat OS cells in vitro. Further research focusing on the potential cytotoxicity of NSAIDs in vivo is needed.
Insights
Nonsteroidal anti-inflammatory drugs (NSAIDs) like ketorolac and indomethacin induce apoptosis in osteosarcoma (OS) cells. This study explored their mechanisms, showing NSAIDs affect key apoptosis markers in OS cells.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Osteosarcoma (OS) is a common pediatric bone cancer.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) are used for pain and inflammation.
- NSAIDs' toxicity in OS is understudied compared to other cancers.
Purpose of the Study:
- Assess ketorolac's apoptosis induction in OS cells.
- Compare ketorolac's effect to indomethacin in OS.
- Investigate the molecular mechanisms of NSAID-induced apoptosis in OS.
Main Methods:
- Used a rat OS cell line (UMR-108).
- Exposed cells to ketorolac and indomethacin.
- Assessed cell viability, apoptosis, and apoptosis-related markers via MTT, colony formation, flow cytometry, gel electrophoresis, and Western blot.
Main Results:
- Ketorolac and indomethacin induced apoptosis in OS cells dose- and time-dependently.
- Apoptosis was confirmed by cell morphology and annexin positivity.
- NSAIDs altered the expression of Bcl-2, survivin, and PARP.
Conclusions:
- NSAIDs effectively induce apoptosis in rat osteosarcoma cells in vitro.
- Further in vivo research is warranted to explore NSAID cytotoxicity in osteosarcoma.
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