Blue light-induced apoptosis of human promyelocytic leukemia cells via the mitochondrial-mediated signaling pathway.

Abstract

Acute promyelocytic leukemia is frequently associated with dizziness, fever, nausea, hematochezia and anemia. Blue light, or light with wavelengths of 400–480 nm, transmits high levels of energy. The aim of the present study was to determine the pro-apoptotic effects of blue light (wavelength, 456 nm; radiation power, 0.25 mW/cm2) and the underlying mechanisms in a human promyelocytic leukemia cell line (HL60). Blue light reduced the viability and enhanced the mortality of HL60 cells in a time-dependent manner. Exposure to blue light for 24 h caused depolarization of the mitochondrial membrane potential and the overproduction of reactive oxygen species in HL60 cells. In a nude mouse model, 9-day exposure to blue light markedly suppressed the growth of HL60-xenografted tumors; however, it had no effect on hepatic and renal tissues. In addition, blue light abrogated the expression of B-cell lymphoma (Bcl)-2 and Bcl extra-long, while enhancing the levels of Bcl-2-associated X protein, cytochrome c, and cleaved caspases-3 and −9 in tumor tissues. The results suggested that the pro-apoptotic effects of blue light in human promyelocytic leukemia cells may be associated with the mitochondrial apoptosis signaling pathway.