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Updated: Jan 22, 2026
Production and Detection of Reactive Oxygen Species ROS in Cancers
Published on: November 21, 2011
Differentiation agents increase the potential AraC therapy of AML by reactivating cell death pathways without
Xuening Wang1, Alaa Dawod2, Matan Nachliely2
1Department of Pathology, Immunology & Laboratory Medicine, Rutgers New Jersey Medical School, State University of New Jersey, Newark, New Jersey.
Abstract:
Acute myeloid leukemia (AML) has a poor prognosis and requires new approaches for treatment. We have reported that a combination of vitamin D-based cell differentiation agents (doxercalciferol/carnosic acid [D2/CA]) added following the cytotoxic drug arabinocytosine (AraC) increases AML cell death (CD), a model for improved therapy of this disease. Because AraC-induced CD is known to involve reactive oxygen species (ROS) generation, here we investigated if the modulation of cellular REDOX status plays a role in the enhancement of cell death (ECD) by D2/CA. Using thiol antioxidants, such as N-acetyl cysteine (NAC), we found a significant inhibition of ECD, yet this occurred in the absence of any detectable change in cellular ROS levels. In contrast, NAC reduced the vitamin D receptor (VDR) abundance and its signaling of ECD. Importantly, VDR knockdown and NAC similarly inhibited ECD without producing an additive effect. Thus, the proposed post-AraC therapy may be compromised by agents that reduce VDR levels in AML blasts.
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