నైరూప్య

Trimethoxy stilbene regulates the nasopharyngeal carcinoma cell apoptosis pathway and enhances sensitization to cisplatin-based chemotherapy

Hua Shao, Ruinian Zheng, Yueming Ding

Objective: Nasopharyngeal carcinoma is a common malignant tumor. This study aims to explore the inhibitory effect and mechanism of trimethoxy stilbene on human nasopharyngeal carcinoma cells.

Methods: Human nasopharyngeal carcinoma cells, CNE1 and 5-8F, in logarithmic phase were collected and inoculated in a 96 pore cell culture plate. Cells were treated with 100 μl of culture media containing 2, 5, 10, or 20 mM of trimethoxy stilbene. MTT was added to each pore after 72 h of continuous cell culture. The absorbance value of each pore was detected at 490 nm by a micro plate reader. CNE1 and 5-8 F cells in logarithmic phase were inoculated in 6 pore cell culture plates. Cells were treated with 100 μl culture media containing 2, 5, 10, or 20 mM of trimethoxy stilbene. Cells cultured for two weeks or 24 h were stained with crystal violet. Photographic images were taken by a digital camera and recorded. Cell cloning was quantitatively analysed with quantity one (Bio-Rad). Annexin V-FITC and PT solution were added to the cell cultures. The mixture was then incubated under ambient temperature for 15 min.

Results: Cisplatin IC₅₀ values of CNE1 and 5-8F cells processed with 20 μmol/L trimethoxy stilbene were evidently lower than that of the control group processed with 0 μmol/L trimethoxy stilbene. In addition, treatment with combined cisplatin and trimethoxy stilbene induced higher rates of apoptosis in CNE1 and 5-8F cells compared with only trimethoxy stilbene or cisplatin. The proportion of cells in G0/G1 phase increased as drug concentration increased. A concentration-effect relationship was observed, indicating that trimethoxy stilbene induced G2/M phase arrest in drug-resistant nasopharyngeal carcinoma cells.

Conclusion: Trimethoxy stilbene significantly inhibited the in-vitro proliferation capacity and clone formation ability of nasopharyngeal carcinoma cells. This inhibitory effect might be realized by inducing nasopharyngeal carcinoma cells to enter G2/M arrest.