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

Author:

Chen Mei‐Chih12ORCID,Yang Bing‐Ze3,Kuo Wei‐Wen4ORCID,Wu Shih‐Hsin3,Wang Tso‐Fu5,Yeh Yu‐Lan6,Chen Ming‐Cheng78,Huang Chih‐Yang39101112ORCID

Affiliation:

1. Department of Medical Research, Translational Cell Therapy Center China Medical University Hospital Taichung Taiwan

2. Department of nursing Asia University Taichung Taiwan

3. Graduate Institute of Biomedical Sciences China Medical University Taichung Taiwan

4. Department of Biological Science and Technology China Medical University Taichung Taiwan

5. Department of Hematology and Oncology Hualien Taiwan

6. Department of Pathology Changhua Christian Hospital Changhua Taiwan

7. Division of Colorectal Surgery, Department of Surgery Taichung Veterans General Hospital Taichung Taiwan

8. College of Medicine National Yang Ming Chiao Tung University Taipei Taiwan

9. Cardiovascular and Mitochondrial Related Disease Research Center, Hualien Tzu Chi Hospital Buddhist Tzu Chi Medical Foundation Hualien Taiwan

10. Department of Science, Holistic Education Center, Buddhist Tzu Chi Medical Foundation Tzu Chi University of Science and Technology Hualien Taiwan

11. Department of Medical Research, China Medical University Hospital China Medical University Taichung Taiwan

12. Department of Medical Laboratory Science and Biotechnology Asia University Taichung Taiwan

Abstract

AbstractResistance to chemotherapy is the deadlock in cancer treatment. In this study, we used wild‐type LOVO (LOVOWT), a human colon cancer cell line, and the oxaliplatin‐resistant sub‐clone LOVOOR cells to investigate the molecular mechanisms of the development of drug resistance in colon cancer. Compared with LOVOWT cells, LOVOOR 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 LOVOOR cells than in LOVOWT cells. The results from immunofluorescence indicated an irregular distribution of Aurora‐A in LOVOOR cells. To evaluate the importance of Aurora‐A in oxaliplatin‐resistant property of LOVOOR cells, overexpression of Aurora‐A in LOVOWT cells and otherwise knockdown of Aurora‐A in LOVOOR cells were performed and followed by administration of oxaliplatin. The results indicated that Aurora‐A might contribute to the resistance of LOVOOR 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.

Publisher

Wiley

Subject

Cell Biology,Molecular Biology,Biochemistry

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