The effects of narrow-band middle infrared radiation in enhancing the antitumor activity of paclitaxel

<p>Paclitaxel is used as an adjuvant to enhance the effectiveness of ionization radiation therapy; however, high-energy radiation often damages the healthy cells surrounding cancer cells. Low-energy, middle-infrared radiation (MIR) has been shown to prevent tissue damage, and recent studies have begun combining MIR with paclitaxel. However, the cytotoxic effects of this treatment combination remain unclear, and the mechanism underlying its effects on HeLa cells has yet to be elucidated. This study investigated the effectiveness of treating HeLa human cervical cancer cells with a combination of paclitaxel for 48 h in conjunction with narrow-band MIR from 3.0 to 5.0 μm. This combined treatment significantly inhibited the growth of HeLa cells. Specifically, results from Annexin V-FITC/PI apoptosis detection and cell mitochondrial membrane potential analyses revealed an increase in apoptotic cell death and a collapse of mitochondrial membrane potential. One possible mechanism underlying cellular apoptosis is an increase in oxidative stress. These preliminary findings provide evidence to support the combination of narrow-band MIR with paclitaxel as an alternative approach in the treatment of human cervical cancer.</p

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

<div><p>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 G₂/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 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.</p> </div

The MIR emitter.

<p>(A) The side view of wide band blackbody source. (B) Schematic diagram showing the setup for the MIR irradiation experiment. The cells were plated onto 12-well plates and cultured in an incubator with 100% humidity, at 37°C and with 5% CO₂.</p

MIR exposure induced G₂/M cell cycle arrest in A549 cells.

<p>Cells were exposed to MIR for 48 h, and harvested for RNA and protein extraction. (A) Gene expression of genes involved in regulation of G₂/M transition (x-axis). The y-axis indicates the relative transcript quantities calculated using the ΔΔCt method with GAPDH as the reference gene amplified from each sample. The data are presented as mean ± S.D. (<i>n</i> = 3). * <i>P</i><0.05, ** <i>P</i><0.001. (B) Protein expression levels were examined by Western blot with actin as the internal control. All experiments were repeated three times. (C) Flow cytometric analysis of DNA content. Cells were exposed to MIR for 48 h. Cells from six independent experiments were collected for analyzing cell cycle distribution. (D) The percentage of cells in each phase was obtained by MultiCycle analysis.</p

Primers used in qPCR.

<p>Primers used in qPCR.</p

Effect of MIR exposure on the actin filaments and focal adhesions of A549 cells.

<p>Cells were seeded onto glass coverslips in 12-well plates, exposed to MIR for 48 hours, fixed for staining and visualized by fluorescence microscopy. Actin filaments were tagged with rhodamine-labeled phalloidin (red), vinculin was labeled with mouse anti-vinculin antibody and the corresponding FITC– conjugated secondary anti-mouse IgG antibody (green), and nuclei were stained with DAPI (blue). Scale bar represents 10 µm. Arrows indicate the position of vinculin.</p

Effect of MIR exposure on the microtubule networks of A549 cells.

<p>Cells were seeded onto glass coverslips in 12-well plates, exposed to MIR for 48 hours, fixed for staining and visualized by fluorescence microscopy. Microtubules were labeled with α–tubulin antibody and the corresponding FITC–conjugated secondary antibody (green), and nuclei were labeled with DAPI (blue). Scale bar represents 10 µm.</p

All-Printed Paper Memory

We report the memory device on paper by means of an all-printing approach. Using a sequence of inkjet and screen-printing techniques, a simple metal–insulator–metal device structure is fabricated on paper as a resistive random access memory with a potential to reach gigabyte capacities on an A4 paper. The printed-paper-based memory devices (PPMDs) exhibit reproducible switching endurance, reliable retention, tunable memory window, and the capability to operate under extreme bending conditions. In addition, the PBMD can be labeled on electronics or living objects for multifunctional, wearable, on-skin, and biocompatible applications. The disposability and the high-security data storage of the paper-based memory are also demonstrated to show the ease of data handling, which are not achievable for regular silicon-based electronic devices. We envision that the PPMDs manufactured by this cost-effective and time-efficient all-printing approach would be a key electronic component to fully activate a paper-based circuit and can be directly implemented in medical biosensors, multifunctional devices, and self-powered systems

Effect of MIR exposure on DNA double strain breaks in A549 cells.

<p>Cells were seeded onto the glass coverslip in 12-well plate, exposure by MIR for 48 hours in the presence or absence of 10 mM N-Acetyl-Cysteine (NAC). Cells were treated with NAC for 1 h prior to MIR exposure (NAC 1 h) or cotreated throughout the exposure for 48 h (NAC). Cells were fixed for staining and visualized by fluorescence microscopy. 53BP1 was labeled with rabbit anti-53BP1 antibody and corresponded FITC–conjugated anti-rabbit IgG antibody (green), γ-H2AX was labeled with mouse anti-γ-H2AX antibody following corresponded PE–conjugated anti-mouse IgG antibody (red), and nuclei were labeled with DAPI (blue). Scale bar represents 10 µm.</p

Quantitative Proteomics Reveals Middle Infrared Radiation-Interfered Networks in Breast Cancer Cells

Breast cancer is one of the leading cancer-related causes of death worldwide. Treatment of triple-negative breast cancer (TNBC) is complex and challenging, especially when metastasis has developed. In this study, we applied infrared radiation as an alternative approach for the treatment of TNBC. We used middle infrared (MIR) with a wavelength range of 3–5 μm to irradiate breast cancer cells. MIR significantly inhibited cell proliferation in several breast cancer cells but did not affect the growth of normal breast epithelial cells. We performed iTRAQ-coupled LC–MS/MS analysis to investigate the MIR-triggered molecular mechanisms in breast cancer cells. A total of 1749 proteins were identified, quantified, and subjected to functional enrichment analysis. From the constructed functionally enriched network, we confirmed that MIR caused G₂/M cell cycle arrest, remodeled the microtubule network to an astral pole arrangement, altered the actin filament formation and focal adhesion molecule localization, and reduced cell migration activity and invasion ability. Our results reveal the coordinative effects of MIR-regulated physiological responses in concentrated networks, demonstrating the potential implementation of infrared radiation in breast cancer therapy