The involvement of Aurora-A and p53 in oxaliplatin-resistant colon cancer cells.

Resistance to chemotherapy is the deadlock in cancer treatment. In this study, we used wild-type LOVO (LOVO ), a human colon cancer cell line, and the oxaliplatin-resistant sub-clone LOVO cells to investigate the molecular mechanisms of the development of drug resistance in colon cancer. Compared with LOVO cells, LOVO cells had a high proliferation capacity and a high percentage on the G2/M phase. The expression and activation of Aurora-A, a critical kinase in G2/M phase, were higher in LOVO cells than in LOVO cells. The results from immunofluorescence indicated an irregular distribution of Aurora-A in LOVO cells. To evaluate the importance of Aurora-A in oxaliplatin-resistant property of LOVO cells, overexpression of Aurora-A in LOVO cells and otherwise knockdown of Aurora-A in LOVO cells were performed and followed by administration of oxaliplatin. The results indicated that Aurora-A might contribute to the resistance of LOVO cells to oxaliplatin treatment by depressing p53 signaling. The specific findings in this study provide a possibility that targeting Aurora-A might be a solution for patients who have failed oxaliplatin treatment.