Department of Life Science, Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan.
PLoS One. 2013;8(1):e54117. doi: 10.1371/journal.pone.0054117. Epub 2013 Jan 15.
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.
有研究探讨了宽带红外辐射（IR）对癌细胞的影响，而中红外辐射（MIR）的影响尚不清楚。在这项研究中，开发了一种发射波长在 3-5 µm 区域的 MIR 发射器，以辐照 A549 肺腺癌细胞。结果发现，MIR 暴露通过改变细胞骨架成分的细胞分布抑制细胞增殖并诱导形态变化。通过定量 PCR，我们发现 MIR 促进了 ATM（共济失调毛细血管扩张突变）、ATR（共济失调毛细血管扩张和 Rad3 相关和 Rad3 相关）、TP53（肿瘤蛋白 p53）、p21（CDKN1A，细胞周期蛋白依赖性激酶抑制剂 1A）和 GADD45（生长停滞和 DNA 损伤诱导）的表达水平，但降低了细胞周期蛋白 B 编码基因 CCNB1 和 CCNB2 以及 CDK1（细胞周期蛋白依赖性激酶 1）的表达水平。CDC25C、cyclin B1 的蛋白表达水平降低以及 CDK1 在 Thr-161 处的磷酸化共同表明 MIR 导致 A549 细胞发生 G2/M 期阻滞。MIR 处理诱导 DNA 双链断裂（DSB）标志物 γ-H2AX 和传感器 53BP1 的 DNA 修复焦点形成，这表明 MIR 诱导的 G2/M 细胞周期阻滞是由 DSB 引起的。本研究通过引发 DSB 和阻断细胞周期进程，说明了 MIR 在肺癌治疗中的潜在作用。
