Overexpression of p67phox in Response to Fluoropyrimidines in HCT116 Cells

Öz

Objectives: Cancer cells require reactive oxygen species (ROS) in order to keep up with growth rate. The accumulation of ROS induced by anticancer drugs can promote cell death through oxidative damage. A potential source of ROS is the family of NADPH oxidase (NOX) enzyme that produces ROS as their sole function. In this study, we aimed to investigate expression of NOX1 and NOX2 subunits in response to fluoropyrimidines in human colon cancer cell line, HCT116.

Methods: We used fluoropyrimidines, 5-fluorouracil (FUra) and 5’-fluoro-2’-deoxyuridine (FdUrd) as anticancer drugs, and measured mRNA levels of NOX1 and NOX2 with semi-quantitative polymerase chain reaction (PCR), quantitative PCR (qPCR) and microarray assays in order.

Results: We found that expression of none of enzyme subunits was altered in response to FUra or FdUrd, except expression of p67phox. Expression of p67phox was induced by drugs approximately 25-fold relative to basal level.

Conclusion: p67phox subunit may be a key subunit in NOX-mediated ROS production following exposure to drugs.

Anahtar Kelimeler

• NADPH Oxidase,p67phox,ROS,colon cancer

Kaynakça

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