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Esophageal cancer is a common malignancy with a high mortality rate. Thelack of effective chemotherapy and a means to overcome drug resistance leads tothe predictable failure of esophageal cancer treatment. Mitotic checkpoint proteinsplay a critical role in regulating the cell cycle and proliferation. Abnormalexpression of the mitotic checkpoint protein BubR1 has been reported in severaltypes of cancers. In this study, we investigated the role of BubR1 in conferringresistance of esophageal cancer cells to anti-microtubule drugs. Using quantitativereal-time PCR analysis on 50 samples of paired esophageal squamous cell cancer(ESC) tissues and adjacent non-cancerous tissues, we found that 72% (36 of 50)of the analyzed ESC samples exhibited high expression levels of BubR1, which wasalso confirmed in ESC cell lines. ESC cells with high levels of BubR1 were lesssensitive to the anti-microtubule drugs paclitaxel and nocodazole. Recombinantadenovirus-mediated enforced expression of BubR1 in relatively sensitive ESC celllines resulted in increased resistance to paclitaxel. Conversely, RNAi-mediatedknockdown of BubR1 restored ESC cell sensitivity to paclitaxel. Cell cycle analysisindicated that the sub-G1 population increased in the ESC cells with reduced BubR1levels. Taken together, our results suggest that upregulation of BubR1 expressionmay be associated with ESC resistance to paclitaxel treatment. Thus, BubR1 mayserve as a potential chemosensitizing target to overcome chemoresistance.

oncology reports

Abnormal expression of the mitotic checkpoint protein BubR1 contributes to the anti-microtubule drug resistance of esophageal squamous cell carcinoma cells