Abstract

The cell viability and apoptosis of tumor U937 cells treated by blue light (BL) irradiation have been examined. BL irradiation can specially inhibit the proliferation and promote the apoptosis of U937 cells, relating to the production of reactive oxygen species (ROS) and the decline of mitochondrial membrane potential (ΔΨm). The apoptosis is further associated with varying downregulated B-cell lymphoma-extra large (Bcl-XL) and B-cell lymphoma 2 (Bcl-2) genes, upregulated Bcl-2-associated X (Bax) gene, the activation of caspase-3 and caspase-9, and the cleavage of poly (ADP-ribose) polymerase (PARP) by the BL irradiation process. Moreover, BL irradiation induced proliferation inhibition is higher than that treated by a common chemotherapeutic drug of homoharringtonine (HHT). When we synergize BL irradiation with HHT (BL-HHT), a higher proliferation inhibition is obtained than that treated by BL irradiation or HHT alone. These results are helpful for establishing a low toxicity and high efficiency strategy of BL irradiation for clinical treatment of acute myeloid leukemia, not limited to U937 cells.

Highlights

  • Acute myeloid leukemia (AML) is a group of hematopoietic malignancies arising from the abnormalities of proliferation, differentiation, or survival of myeloid progenitors [1]

  • We further investigate the possible role of blue light (BL) irradiation in controlling the apoptosis of U937 cells cells through the activation of caspase proteins

  • The cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) treated by irradiation are 3.1 (1.1) and 2.0 times higher than that treated by HHT. These results suggest that the BL irradiation enhances proliferation inhibition of U937 cells by improving the activation of caspase-3 and caspase-9, and cleavage of PARP, which is more efficient than in those treated by the performed onHHT

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Summary

Introduction

Acute myeloid leukemia (AML) is a group of hematopoietic malignancies arising from the abnormalities of proliferation, differentiation, or survival of myeloid progenitors [1]. To improve leukemia treatment and decrease the side effects, the composite medicines are prepared to obtain high complete remission rate [7,10], while long time cytarabine or aclarubicin treatment are always accompanied with fatal complications [11]. Another strategy is introducing nanomaterials as a form of drug delivery that can increase the bioavailability and solubility of the drugs [12], but it is difficult to avoid toxicity [13] and aggregation [14] related to small-sized nanomaterials. It is highly desirable to explore a new strategy to further improve therapeutic efficiency and minimize side effects in the treatment of U937 cells

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