Abstract
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 µm 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 γ-H2AX and sensor 53BP1 was induced by MIR treatment, it implies the MIR induced G(2)/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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / metabolism
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CDC2 Protein Kinase / metabolism
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Cell Culture Techniques
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Cell Cycle Proteins / genetics
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Cell Line, Tumor
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Cell Proliferation / radiation effects
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Culture Media
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Cyclin B1 / genetics
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DNA Damage / radiation effects
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G2 Phase Cell Cycle Checkpoints / genetics
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G2 Phase Cell Cycle Checkpoints / radiation effects*
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Gene Expression Regulation, Neoplastic / radiation effects
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Histones / metabolism
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Humans
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Infrared Rays*
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Intracellular Signaling Peptides and Proteins / metabolism
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Lung Neoplasms / metabolism
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M Phase Cell Cycle Checkpoints / genetics
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M Phase Cell Cycle Checkpoints / radiation effects*
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Microtubules / metabolism
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Phosphorylation / radiation effects
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Protein Binding
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Protein Transport / radiation effects
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RNA, Messenger / genetics
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Reactive Oxygen Species / metabolism
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Temperature
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Tumor Suppressor p53-Binding Protein 1
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Vinculin / metabolism
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cdc25 Phosphatases / genetics
Substances
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Actins
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Cell Cycle Proteins
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Culture Media
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Cyclin B1
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H2AX protein, human
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Histones
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Intracellular Signaling Peptides and Proteins
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RNA, Messenger
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Reactive Oxygen Species
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TP53BP1 protein, human
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Tumor Suppressor p53-Binding Protein 1
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Vinculin
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CDC2 Protein Kinase
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cdc25 Phosphatases
Grants and funding
This work was supported by the National Science Council, Taiwan (NSC 100-2120-M-002-014, NSC 99-2621-B-002-005-MY3, NSC 99-2621-B-010-001-MY3) and National Taiwan University Cutting-Edge Steering Research Project (10R70602C3 and 101R4000). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.