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Published on: March 18, 2014
Differential Sensitivity of Taxol-induced Apoptosis in U2OS and SaOS2 Osteogenic Sarcoma Cells
Purpose:
Taxol (Paclitaxel) is a new generation of chemotherapeutic drug proven to be effective in the treatment of many cancers. In this study, to further demonstrate the differential effect of the tumor suppressor gene, p53, on the Taxol-induced apoptosis in osteogenic sarcoma cell lines, we used p53-defected SaOS2 cells and wild type p53-expressed U2OS cells.
Materials And Methods:
The cell viability was measured by the XTT assay. To examine whether the differential expressions of p53, in U2OS and SaOS2 cells, were associated with Taxol-induced apoptosis, DNA fragmentation assays were performed on both cytosolic and genomic DNA. Since the cleavage of poly (ADP-ribose) polymerase (PARP) is primarily responsible for apoptosis, the cleavage of PARP, and the expression of cyclin B1, polo-like kinase, Bax, Bcl-xL, Bcl-2 in U2OS and SaOS2 cells were compared by Western blot analyses.
Results:
The cell viability of the p53-defected SaOS2 cells was markedly decreased with Taxol treatment. Whereas, the cell viabilities due to 6-mercaptopurine and adriamycin were no different between the U2OS and SaOS2 cells. Treatment with Taxol induced a ladder- like pattern of DNA fragments, which is a biochemical hallmark of apoptosis, consisting of multiples of approximately 180-200 base pairs, in a dose-dependent manner in the SaOS2 cells, but insignificantly with the U2OS cells. When the cells were treated with Taxol, the 89 kDa cleavage product of PARP clearly appeared as a function of time in the SaOS2 cells, but not in the U2OS cells. The Taxol-induced apoptosis in p53 defected-osteogenic sarcoma cells was associated with the PARP cleavage as a result of the increased activity of caspase 3, and the high expressions of cyclin B1 and PLK. Bax, as a proapoptotic factor, was increased in the SaOS2cells, but the Bcl-xL and Bcl-2 were decreased when the cells were exposed to 10miceoM Taxol.
Conclusion:
From these results, it was concluded that p53-defected SaOS2 cells are much more sensitive to Taxol-induced apoptosis than p53-expressed U2OS cells.
Insights
Osteosarcoma cells lacking the p53 tumor suppressor gene are more sensitive to Taxol-induced apoptosis. This study highlights p53
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Taxol (Paclitaxel) is a key chemotherapeutic agent.
- The tumor suppressor gene p53 plays a role in cancer treatment response.
- Osteosarcoma is a bone cancer with various treatment strategies.
Purpose of the Study:
- To investigate the differential effect of p53 on Taxol-induced apoptosis in osteosarcoma.
- To compare Taxol sensitivity in p53-deficient (SaOS2) versus p53-expressing (U2OS) cells.
Main Methods:
- Cell viability assessed using XTT assay.
- DNA fragmentation assays to detect apoptosis.
- Western blot analysis for apoptosis-related proteins (PARP, cyclin B1, PLK, Bax, Bcl-xL, Bcl-2).
Main Results:
- p53-deficient SaOS2 cells showed significantly decreased viability with Taxol.
- Taxol induced DNA fragmentation and Poly (ADP-ribose) polymerase (PARP) cleavage in SaOS2 cells, but not U2OS cells.
- Apoptosis in SaOS2 cells involved increased caspase 3 activity, cyclin B1, polo-like kinase (PLK), and altered Bax/Bcl-2 expression.
Conclusions:
- p53-deficient osteosarcoma cells are more sensitive to Taxol-induced apoptosis.
- p53 status influences the response to Taxol chemotherapy in osteosarcoma.
