Journal
JOURNAL OF ONCOLOGY
Volume 2022, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2022/8281267
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Funding
- Capacity Improvement Project of Medical Institutions Directly Under Henan Province [2017.66]
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This study found that deferoxamine (DFO) effectively reduced the concentration of intracellular iron in ALL cells, inhibiting cell proliferation and inducing apoptosis. The combination of DFO and dextriferron (Dex) decreased the sensitivity of ALL cells to DFO. Additionally, DFO inhibited tumor growth in mice and affected multiple signaling pathways involved in cell cycle regulation and cell survival.
Acute lymphoblastic leukemia (ALL) is the most common type of childhood cancer, with a feature of easy to induce multidrug resistance and relapse. Abundant studies have proved that iron overload strengthens the growth and metastasis of tumor cells. Herein, we found that deferoxamine (DFO) effectively decreased the concentration of intracellular iron in ALL cells. DFO inhibited proliferation, induced apoptosis, and obstructed cell cycle of ALL cells, whereas DFO and dextriferron (Dex) used in combination significantly decreased the sensitivity of ALL cells to DFO. Reactive oxygen species (ROS) level was reduced in ALL cells treated with DFO, and the combination of DFO and Dex reversed the effects of DFO. In vivo, DFO inhibited mouse tumor growth. Besides, cyclinD1, beta-catenin, c-Myc, hypoxia inducible factor 1 (HIF-1), p-p38MAPK, and p-ERK1/2 protein levels were significantly downregulated, and the levels of prolyl hydroxylase-2 (PHD-2) were upregulated after treated with DFO, whereas Dex treatment reversed those in vivo and in vitro. In conclusion, DFO inhibited the proliferation and ALL xenograft tumor growth, obstructed the cell cycle, and induced apoptosis of ALL cells, probably via inactivating the ROS/HIF-1 alpha, Wnt/beta-catenin, and p38MAPK/ERK signaling.
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