Middle Infrared Radiation Induces G2/M Cell Cycle Arrest in A549 Lung Cancer Cells

被引:31
作者
Chang, Hsin-Yi [1 ]
Shih, Meng-Her [1 ]
Huang, Hsuan-Cheng [2 ]
Tsai, Shang-Ru [3 ]
Juan, Hsueh-Fen [1 ,3 ]
Lee, Si-Chen [3 ,4 ]
机构
[1] Natl Taiwan Univ, Dept Life Sci, Inst Mol & Cellular Biol, Taipei 10764, Taiwan
[2] Natl Yang Ming Univ, Inst Biomed Informat, Ctr Syst & Synthet Biol, Taipei 112, Taiwan
[3] Natl Taiwan Univ, Grad Inst Biomed Elect & Bioinformat, Taipei 10764, Taiwan
[4] Natl Taiwan Univ, Dept Elect Engn, Taipei 10764, Taiwan
关键词
DNA-DAMAGE RESPONSE; OXIDATIVE STRESS; SINGLET OXYGEN; ACTION SPECTRA; HUMAN SKIN; ULTRAVIOLET; INDUCTION; PATHWAY; KINASE; REPAIR;
D O I
10.1371/journal.pone.0054117
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
There were studies investigating the effects of broadband infrared radiation (IR) on cancer cell, while the influences of middle-infrared radiation (MIR) are still unknown. In this study, a MIR emitter with emission wavelength band in the 3-5 mu m region was developed to irradiate A549 lung adenocarcinoma cells. It was found that MIR exposure inhibited cell proliferation and induced morphological changes by altering the cellular distribution of cytoskeletal components. Using quantitative PCR, we found that MIR promoted the expression levels of ATM (ataxia telangiectasia mutated), ATR (ataxia-telangiectasia and Rad3-related and Rad3-related), TP53 (tumor protein p53), p21 (CDKN1A, cyclin-dependent kinase inhibitor 1A) and GADD45 (growth arrest and DNA-damage inducible), but decreased the expression levels of cyclin B coding genes, CCNB1 and CCNB2, as well as CDK1 (Cyclin-dependent kinase 1). The reduction of protein expression levels of CDC25C, cyclin B1 and the phosphorylation of CDK1 at Thr-161 altogether suggest G(2)/M arrest occurred in A549 cells by MIR. DNA repair foci formation of DNA double-strand breaks (DSB) marker gamma-H2AX and sensor 53BP1 was induced by MIR treatment, it implies the MIR induced G2/M cell cycle arrest resulted from DSB. This study illustrates a potential role for the use of MIR in lung cancer therapy by initiating DSB and blocking cell cycle progression.
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页数:9
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