Background and purpose: Aurora A kinase (Aurora A)

a member of serine/threonine kinase family

contributes to chemo-resistance in ovarian cancer. Reactive oxygen species (ROS)

generated during

normal metabolism in aerobic organisms

are involved in multiple signaling pathways. Cancer cells possess higher ROS levels than normal cells due to the increased metabolism and cellular redox imbalance. Moreover

ROS levels are lower in chemo-resistant cells

suggesting the crucial role of ROS in chemo-resistance. However

the role of ROS in Aurora A-mediated chemo-resistance is largely unexplored. Methods: ROS levels of A2780 and A2780/CDDP were examined using 2’

7’-dichlorofluorescin diacetate (DCFH-DA)

and 50% inhibitory concentration (IC50) values of cisplatin were measured by methyl thiazolyl tetrazolium (MTT). Establishment of stable ovarian cancer cell lines harboring Aurora A cDNA or shRNA were conducted by Lentil-virus infection and subsequent drug screening. ROS levels and IC

50

 values of cisplatin were detected in these established cells. IC

50

values of cisplatin were also measured in combination with N-acetyl-L-cysteine (NAC). To explore the potential mechanism

cells were collected and subjected to Western blot. Results: Chemo-resistant cells exhibited lower ROS levels than control cells. Reduction of ROS levels by NAC promoted chemo-resistance. Overexpression of Aurora A inhibited ROS and conferred chemo-resistance. Knockdown of Aurora A elevated the ROS levels and promoted chemo-sensitivity. Aurora A promoted the phosphorylation of AMPactivated protein kinase (AMPK) and glycolysis. Conclusion: Aurora A promotes chemo-resistance by decreasing the cellular ROS levels. AMPK phosphorylation and glycolysis are involved in Aurora A-mediated ROS regulation.