The Phase Distribution Of Cell Cycle In Parental And Taxol-resistant Nasopharyngeal Carcinoma

Objective:To detect the phase distribution of cell cycle in parental and taxol-resistent nasopharyngeal carcinoma, and determine the changes of cell cycle regulatorsMethod:1. The colony formation assay was repeatly carried out to detect the resistance index of paclitaxel-resistance nasopharyngeal carcinoma cells(CNE-1/Taxol, HNE-2/Taxol and 5-8F/Taxol).2. The cell cycle distribution was detected by flow cytometry when cells were treated with or without different concentrations of paclitaxel and cisplatin in parental cell line and the paclitaxel resistant cell line.3. The expression of CDK1 and BubRl were detected by Quantitative RT-PCR in the parental and taxol resistant cells of nasopharyngeal carcinoma.Results:1. G2/M arrest appeared in CNE-1 cell treated with 10ng/ml paclitaxel, and it was increased in a dose-dependent way. G2/M arrest also appeared in CNE-1/Taxol with 15ng/ml paclitaxel, and it was increased in a dose-dependent way. The percentage of G2/M arrest in CNE-1 was significantly higher than in CNE-1/taxol when both cell lines treated with the same concentration of paclitaxol (10-50 ng/ml), (p<0.05).2. The S phase arrest showed in both CNE-1 and CNE-1/Taxol cells treated by Cisplatin. However, the percentage of S arrest was significantly higher in CNE-1/taxol than in CNE-1 cells when both cells treated with the same concentration of cisplatin (p<0.05).3.The expression of CDK1 in the paclitexal resistant NPC cells was 3-fold higher than in the parental NPC cells. However, the expression level of BubRl was almost the same in both cell lines.Conclusions:1. The distribution of cell cycle phase was not changed when nasopharyngeal carcinoma cells were induced into paclitaxel-resistent cells. However, the lowest concentration was significantly increased when the G2/M arrest appeared in taxol resistent cells treated with paclitaxel, and significantly decreased when S phase arrest appeared in taxol resistent cells treated with cisplatin.2. The changes of drug concentrations caused G2/M and S arrest in taxol resistent cells might relate to upregulation of CDK1 expression, a key protein of cell cycle. However, it was not associated with BubRl expression.