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[Molecular mechanism of radiosensitizing effect of paclitaxel]
Wan-Wen Weng1, Yu-Jie Xu, Jian-Mei Wan
1Department of Basic Nuclear Medicine, School of Radiation Medicine and Public Health, Medical College of Soochow University, Suzhou, Jiangsu, 215123, P.R. China.
Background & Objective:
Paclitaxel is a radiosensitizer which may stabilize microtubules, block the G2/M phase of the cell cycle and thus modulate the radioresponsiveness of tumor cells. However, its potential molecular mechanisms of radiosensitization have not been well understood yet. This study was to investigate the radiosensitizing effect of paclitaxel on human oral epithelium carcinoma (KB) cell line and to explore the molecular mechanism of radiosensitization.
Methods:
The survival of KB cells following the treatment with paclitaxel and/or radiation was determined by colony-forming assay. The radiosensitizing effect was evaluated by calculating the sensitizing enhancement ratio (SER) with multi-target single hit model. The cell cycle distribution was analyzed by flow cytometry. Differentially expressed genes related to paclitaxel radiosensitization were screened using human Oligo microarray. Expressions of protein regulating cytokinesis 1 (PRC1) and cyclin B2 genes were confirmed by real-time quantitative PCR.
Results:
The proliferation of KB cells was significantly inhibited by paclitaxel combined with ionizing radiation. The SERD0 and SERDq were (2.40 +/- 1.87) and (12.23 +/- 2.81) respectively, when the concentration of paclitaxel was 20 nmol/l. After the treatment with paclitaxel in combination with irradiation, the percentage of G1 phase cells decreased from (48.32 +/- 2.40)% to (15.73 +/- 7.00)% (P<0.01), and the percentage of G2/M phase cells increased from (13.66 +/- 2.16)% to (52.51 +/- 5.02)% (P<0.01). In total 176 differentially expressed genes were identified to be related to paclitaxel radiosensitization. Ten genes were found to regulate cell division, two of which were up-regulated and eight were down-regulated after the treatment. Moreover, the expression of PRC1 and cyclin B2 was decreased.
Conclusion:
The radiosensitizing effect of paclitaxel on KB cells may be due to the down-regulated expression of PRC1 and cyclin B2, resulting in inhibition of mitotic spindle formation and cell necrosis.
Insights
Paclitaxel enhances radiation therapy by inhibiting oral cancer cell growth. This radiosensitizing effect is linked to decreased expression of PRC1 and cyclin B2, disrupting cell division and promoting cell death.
Area of Science:
- Oncology
- Molecular Biology
- Radiotherapy
Context:
- Paclitaxel is a known radiosensitizer, but its precise molecular mechanisms remain unclear.
- Oral epithelium carcinoma (KB) cells are used to investigate radiosensitization.
- Understanding these mechanisms can improve cancer treatment strategies.
Purpose:
- To evaluate the radiosensitizing effect of paclitaxel on human oral epithelium carcinoma (KB) cells.
- To elucidate the molecular mechanisms underlying paclitaxel-induced radiosensitization.
Summary:
- Paclitaxel combined with ionizing radiation significantly inhibited KB cell proliferation.
- The sensitizing enhancement ratio (SER) indicated a notable radiosensitizing effect.
- Paclitaxel treatment increased G2/M phase arrest and decreased G1 phase cells.
- Gene expression analysis revealed differential regulation of cell division genes, including down-regulated PRC1 and cyclin B2.
Impact:
- Paclitaxel demonstrates significant radiosensitizing potential in oral cancer cells.
- Down-regulation of PRC1 and cyclin B2 contributes to paclitaxel's radiosensitizing effect.
- This suggests paclitaxel may inhibit mitotic spindle formation, leading to cell necrosis and improved therapeutic outcomes.
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