title: Millimeter wave treatment induces apoptosis via activation of the mitochondrial-dependent             pathway in human osteosarcoma cells.
abstract: Millimeter wave (MW) is an electromagnetic wave with a wavelength between             1 and 10 mm and a frequency of 30-300 GHz that causes multiple biological effects             and has been used as a major component in physiotherapies for the clinical treatment             of various types of diseases including cancers. However, the precise molecular             mechanism of the anticancer activity of millimeter wave remains to be elucidated.             In the present study, we investigated the cellular effects of the MW in the U-2OS             human osteosarcoma cell line. Our results showed that MW induced cell morphological             changes and reduced cell viability in a dose- and time-dependent manner suggesting             that MW inhibited the growth of U-2OS cells as demonstrated. Hoechst 33258 staining             and Annexin V/propidium iodide double staining exhibited the typical nuclear features             of apoptosis and increased the proportion of apoptotic Annexin V-positive cells             in a dose-dependent manner, respectively. In addition, MW treatment caused loss             of plasma membrane asymmetry, release of cytochrome c, collapse of mitochondrial             membrane potential, activation of caspase-9 and -3, and increase of the ratio             of pro-apoptotic Bax to anti-apoptotic Bcl-2. Taken together, the results indicate             that the U-2OS cell growth inhibitory activity of MW was due to mitochondrial-mediated             apoptosis, which may partly explain the anticancer activity of millimeter wave             treatment.
authors.affiliation: Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou 350108, PR China.
authors.forename: Guangwen
authors.initials: G
authors.lastname: Wu
authors.forename: Xuzheng
authors.initials: X
authors.lastname: Chen
authors.forename: Jun
authors.initials: J
authors.lastname: Peng
authors.forename: Qiaoyan
authors.initials: Q
authors.lastname: Cai
authors.forename: Jinxia
authors.initials: J
authors.lastname: Ye
authors.forename: Huifeng
authors.initials: H
authors.lastname: Xu
authors.forename: Chunsong
authors.initials: C
authors.lastname: Zheng
authors.forename: Xihai
authors.initials: X
authors.lastname: Li
authors.forename: Hongzhi
authors.initials: H
authors.lastname: Ye
authors.forename: Xianxiang
authors.initials: X
authors.lastname: Liu
mesh_terms: D017209:Apoptosis / Q000528:radiation effects*; D001859:Bone Neoplasms / Q000378:metabolism / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D053453:Caspase 9 / Q000378:metabolism; D045744:Cell Line, Tumor; D048430:Cell Shape / Q000528:radiation effects; D002470:Cell Survival / Q000528:radiation effects; D045304:Cytochromes c / Q000378:metabolism; D004307:Dose-Response Relationship, Radiation; D060733:Electromagnetic Radiation; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000528:radiation effects; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology* / Q000528:radiation effects*; D012516:Osteosarcoma / Q000378:metabolism / Q000473:pathology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D015398:Signal Transduction / Q000528:radiation effects*; D013997:Time Factors; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494826:BAX protein, human; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D045304:Cytochromes c; C505407:CASP3 protein, human; C506433:CASP9 protein, human; D053148:Caspase 3; D053453:Caspase 9