Synergistic anti-tumor effects of arsenic trioxide and blue LED irradiation on human osteosarcoma

Synergistic anti-tumor effects of arsenic trioxide and blue LED irradiation on human osteosarcoma
复制标题

三氧化二砷与蓝光LED照射对人骨肉瘤的协同抗肿瘤作用

DOI:
10.7150/ijbs.28356
复制
发表时间:
2019-01-01
影响因子:
9.2
通讯作者:
Yang, Lei
Yang, Lei
中科院分区:
生物学2区
文献类型:
--
作者:
Feng, Chao;Gong, Rui;Yang, Lei

文献摘要

被引文献

相似文献

三氧化二砷(ATO)已被公认为是多种人类癌症的抗肿瘤剂。最近,基于蓝光发光二极管(LED)的疗法也被证明是几种癌症的潜在治疗策略。然而,ATO和蓝色LED对肿瘤抑制的联合作用仍不清楚。在这项研究中,我们确定ATO和蓝色LED照射在470 nm波长的组合是否在人骨肉瘤(OS)中表现出上级抗肿瘤活性。我们观察到ATO和蓝光LED联合处理比任何单一处理更显著地降低了U-2 OS细胞的增殖百分比,并增加了凋亡率。此外,我们发现ATO+蓝光LED处理组对细胞迁移和侵袭的抑制比单独处理组明显得多。活性氧(ROS)测定和γ-H2 A. X和p53免疫组化结果表明,联合处理可进一步显著增加ROS的积累、DNA损伤和p53活性。综上所述,我们的研究表明ATO和蓝色LED联合处理对人OS细胞的协同抗肿瘤作用,这与ROS积累增加、DNA损伤介导的p53激活有关。
Arsenic trioxide (ATO) has been well recognized as an anti-tumor agent for various human cancers. Recently, the blue light emitting diodes (LEDs)-based therapy has also been demonstrated to be potential therapeutic strategies for several cancers. However, the combination effects of ATO and blue LED on tumor suppression are still unclear. In this study, we determined whether combination of ATO and blue LED irradiation at 470 nm in wavelength exhibited superior anti-tumor activity in human osteosarcoma (OS). We observed that combination treatments of ATO and blue LED much more significantly decreased the percentages of proliferative cells, and increased apoptotic rate compared with any single treatments in U-2 OS cells. Furthermore, we found suppression of cell migration and invasion were much more pronounced in ATO plus blue LED treated group than single treated groups. Moreover, reactive oxygen species (ROS) assay and immunostaining of γ-H2A.X and p53 indicated that the combined treatments resulted in further markedly increases in ROS accumulation, DNA damage and p53 activity. Taken together, our study demonstrated synergistical anti-tumor effects of combined treatments of ATO and blue LED on human OS cells, which were associated with an increased ROS accumulation, DNA damaged mediated p53 activation.