Overexpression of p67phox in Response to Fluoropyrimidines in HCT116 Cells

Yıl 2016, Cilt: 43 Sayı: 4, 490 - 489, 25.12.2016

Ufuk Ozer Karen Wood Barbour

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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