OBJECTIVE: To study the effect of microwave radiation on the levels of malondialdehyde (MDIA) and activity of superoxide dismutase (SOD) of Nasopharyngeal carcinoma cells. METHOD: The experiment were divided into four groups included control, 10, 20 and 30 mW/cm2 groups. The methods, such as TBA colorimetric assay and modified NBT hydroxylamine method, were used to detect the effect of microwave radiation on the levels of MDA and activity of SOD of nasopharyngeal carcinoma cells. RESULT: With increase of microwave radiation, TBA assay showed that the levels of MAD were 1.4 and 3.5 times in 20 mW/cm2 group and 30 mW/cm2 group respectively compared with control group, there were significant differences among them (P < 0.05). NBT method shows that the activity of SOD were 68.2%, 46.2% and 36.0% of 10, 20 and 30 mW/cm2 groups respectively compared with control group, there were significant differences among them too (P < 0.01). CONCLUSION Microwave Radiation could up-regulate the levels of MAD) while down-regulate the SOD activity.
Cell Line, Tumor ; Dose-Response Relationship, Radiation ; Gene Expression Regulation, Neoplastic ; Humans ; Malondialdehyde ; metabolism ; radiation effects ; Microwaves ; Nasopharyngeal Neoplasms ; metabolism ; Superoxide Dismutase ; metabolism ; radiation effects ; Up-Regulation

OBJECTIVETo investigate the effects of radiosensitivity and X-ray dose on the expression of miR-7 in nasopharyngeal carcinoma (NPC) cells.

METHODSLow radiosensitive NPC cells CNE-1 and high radiosensitive NPC cells CNE-2 were exposed to 0, 2 and 8 Gy X-ray. The total RNAs of the cell lines were extracted 10 h after radiation for reverse transcription of miR-7 and 18S rRNA by stem-loop primer and random hexamers, respectively. The non-irradiated CNE-1 cells served as the control sample and the relative quantity of the expression level was calculated after real-time PCR using SyBR green.

RESULTSmiR-7 expression differed significantly between CNE-1 and CNE-2 cells (4.49-/+3.62 vs 1.29-/+1.10, F=135.483, P<0.001). The radiation dose also significantly affected the expression of miR-7 in NPC cells (F=39.565, P<0.001). CNE-1 cells with a 2 Gy exposure had the highest expression level of miR-7, while the non-irradiated CNE-1 cells had the lowest expression. CNE-2 cells exposed to 2 Gy X-ray had the lowest expression level of miR-7 and the non-irradiated CNE-2 cells had the highest.

CONCLUSIONRadiosensitivity and radiation dose of X-ray have significant effect on the expression of miR-7 in NPC cells, indicating that miR-7 plays an important role in radioresistance of NPC cells to X-ray, and suppressed miR-7 expression may elevate the radiosensitivity of NPC cells.

Apoptosis ; radiation effects ; Carcinoma ; Cell Line, Tumor ; Dose-Response Relationship, Radiation ; Gene Expression Regulation, Neoplastic ; radiation effects ; Humans ; MicroRNAs ; genetics ; Nasopharyngeal Neoplasms ; genetics ; Radiation Tolerance ; genetics ; X-Rays

OBJECTIVETo study genome-wide gene expression changes in gastric cancer cells after iodine-125 ¹²⁵(I) particle irradiation.

METHODS¹²⁵I particles were used to irradiate three gastric cancer cell lines of various differentiation levels:high (BGC-823) , medium (AGS) and low (NCI-N87) .Whole-genome gene expression was investigated with microarray. The gene expression in iodine-125 irradiated and untreated cancer cells was compared, and the genes with transcript levels altered for at least 2 folds (P < 0.05) were selected. The change in gene expression levels was verified by using quantitative real-time (qRT) -PCR.

RESULTSThe three gastric cancer cell lines received the same dose rate of ¹²⁵I particle irradiation. Cluster analysis showed that the Gene Ontology (GO) categories did not change in the three cell lines, but changes in gene expression levels were evident for many genes. After ¹²⁵I particle irradiate NCI-N87 cells, 895 genes were up-regulated, 786 genes were down-regulated; AGS was irradiated by ¹²⁵I seed, there were 124 genes upregulated, 161 genes were down-regulated; BGC-823 cells were treated by ¹²⁵I seed irradiation, 2 412 genes upregulated, 3 243 downregulated genes. After ionizing radiation can cause very complex transcriptional regulation changes, KEGG pathway analysis shows that these differentially expressed genes overlap in a particular cell pathway. Four genes, TRAF3IP2-AS1, SDC1, RABL2B and NOM, were found having at least 2-fold difference in expression (P < 0.05) , and the gene expression alteration was confirmed by qRT-PCR.

CONCLUSIONS¹²⁵I particle irradiation caused gene expression changes in gastric cancer cells. The expressions of TRAF3IP2-AS1, SDC1, RABL2B and NOM are altered significantly in all three cell lines studied, indicating that these genes may play an important role in the ¹²⁵I seed treatment of gastric cancer. These genes could be potential targets for developing anti-cancer drugs in the future.

Cell Line, Tumor ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; radiation effects ; Humans ; Iodine Radioisotopes ; adverse effects ; Stomach Neoplasms ; metabolism ; pathology

OBJECTIVETo investigate the effect of curcumin (Cur) on radiosensitivity of nasopharyngeal carcinoma cell CNE-2 and its mechanism.

METHODThe effect of curcumin on radiosensitivity was determined by the clone formation assay. The cell survival curve was fitted by Graph prism 6. 0. The changes in cell cycle were analyzed by flow cytometry (FCM). The differential expression of long non-coding RNA was detected by gene chip technology. Part of differentially expressed genes was verified by Real-time PCR.

RESULTAfter 10 micro mol L-1 Cur had worked for 24 h, its sensitization enhancement ratio was 1. 03, indicating that low concentration of curcumin could increase the radiosensitivity of nasopharyngeal carcinoma cells; FCM displayed a significant increase of G2 phase cells and significant decrease of S phase cells in the Cur combined radiation group. In the Cur group, the GUCY2GP, H2BFXP, LINC00623 IncRNA were significantly up-regulated and ZRANB2-AS2 LOC100506835, FLJ36000 IncRNA were significantly down-regulated.

CONCLUSIONCur has radiosensitizing effect on human nasopharyngeal carcinoma CNE-2 cells. Its mechanism may be related to the changes in the cell cycle distribution and the expression of long non-coding IncRNA.

Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Curcumin ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; radiation effects ; Humans ; RNA, Long Noncoding ; genetics ; Radiation Tolerance ; drug effects

OBJECTIVETo investigate and compare the effect of radio-frequency (RF) field exposure on expression of heat shock proteins (Hsps) in three human glioma cell lines (MO54, A172, and T98).

METHODSCells were exposed to sham or 1950 MHz continuous-wave for 1 h. Specific absorption rates (SARs) were 1 and 10 W/kg. Localization and expression of Hsp27 and phosphorylated Hsp27 ((78) Ser) (p-Hsp27) were examined by immunocytochemistry. Expression levels of Hsp27, p-Hs27, and Hsp70 were determined by Western blotting.

RESULTSThe Hsp27 was primarily located within the cytoplasm, p-Hsp27 in both cytoplasm and nuclei of MO54, A172, and T98 cells. RF field exposure did not affect the distribution or expression of Hsp27. In addition, Western blotting showed no significant differences in protein expression of Hsp27 or Hsp70 between sham- and RF field-exposed cells at a SAR of 1 W/kg and 10 W/kg for 1 h in three cells lines. Exposure to RF field at a SAR of 10 W/kg for 1 h slightly decreased the protein level of phosphorylated Hsp27 in MO54 cells.

CONCLUSIONThe 1950 MHz RF field has only little or no apparent effect on Hsp70 and Hsp27 expression in MO54, A172, and T98 cells.

Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; radiation effects ; Glioma ; Heat-Shock Proteins ; genetics ; metabolism ; Humans ; Neoplasm Proteins ; genetics ; metabolism ; Neuroglia ; radiation effects ; Protein Transport

OBJECTIVETo examine UVB-induced responses in normal human keratinocytes (HaCaT) and epidermoid carcinoma cells (A431) at the cellular and molecular level, and investigated the protective effect of salidroside.

METHODSCells irradiated by UVB at various dosage and their viability was assessed by MTT assays, cell cycle was analysed by flow cytometry. The expression of NF-κB, BCL-2, and CDK6 after 50 J/m(2) UVB irradiation were detected by RT-PCR and western blotting.

RESULTSOur results confirmed greater tolerance of A341 cells to UVB-induced damage such as cell viability and cell cycle arrest, which was accompanied by differential expression changes in NF-κB, BCL-2, and CDK6. UVB exposure resulted in HaCaT cells undergoing G(1)-S phase arrest. When treated with salidroside, HaCaT survival was significantly enhanced following exposure to UVB, suggesting great therapeutic potential for this compound.

CONCLUSIONTaken together, our study suggests that A431 respond differently to UVB than normal HaCaT cells, and supports a role for NF-κB, CDK6, and BCL-2 in UVB-induced cell G(1)-S phase arrest. Furthermore, salidroside can effectively protect HaCaT from UVB irradiation.

Antioxidants ; pharmacology ; Apoptosis ; radiation effects ; Carcinoma, Squamous Cell ; Cell Cycle Checkpoints ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Gene Expression Regulation, Neoplastic ; Glucosides ; pharmacology ; Humans ; Keratinocytes ; radiation effects ; Phenols ; pharmacology ; Ultraviolet Rays

BACKGROUND AND OBJECTIVEVarious factors affect the radioresistance of tumor cells, with unknown molecular mechanism(s). Many genes have been found to associate with the radioresistance of tumor cells, however, the precise mechanism of these genes have not been elucidated. This paper was to analyze the differential expressions of DNA repair genes in esophageal carcinoma cells at different time after X-ray irradiation, and to investigate the role of these DNA repair genes in radiation resistance.

METHODSEsophageal cancer parental cells Seg-1 were treated with continuous 2 Gy of fractionated irradiation until the total dose reached 60 Gy to establish the radioresistant cell line Seg-1R. Total RNA was extracted from each cell line at 0, 8, and 24 h after irradiation. Illumine Human-6 V3 microarray was used to identify differentially expressed genes between parental and radioresistant cells. Ten genes involved in DNA repair were obtained and their expressions at different time points after irradiation were analyzed by Gene Ontology analysis.

RESULTSTen DNA repair associated genes were found to be differentially expressed. Three of these genes, SLK, HMGB1, and PMS1, were not only differentially expressed between parental and radioresistant cell lines, but also expressed differently at different time points after irradiation in the same cell line.

CONCLUSIONSPMS1 may be an important factor involved in the mechanism of radioresistance of esophageal carcinoma cells.

Cell Line, Tumor ; radiation effects ; DNA Repair ; genetics ; DNA, Neoplasm ; genetics ; Esophageal Neoplasms ; genetics ; pathology ; Gene Expression Regulation, Neoplastic ; radiation effects ; Humans ; MutL Proteins ; Neoplasm Proteins ; genetics ; metabolism ; Oligonucleotide Array Sequence Analysis ; Radiation Tolerance ; Transcriptome ; X-Rays

OBJECTIVETo explore the increasing effect of blocking Chk1 and /or Chk2 gene by Chk1 or Chk2-specific antisense oligodeoxynucleotides (AsODN) on apoptosis in HeLa cell line after irradiation and its mechanism of action.

METHODSAsynchronized HeLa cells were exposed to (60)Co-irradiation at different dosage to activate G(2)/M checkpoint arrest. The cell cycle profiles were observed in HeLa cells after irradiation at a range of various doses and different time points by flow cytometry. In the experimental groups, Chk1/2 sODN and AsODN alone or in combination were transfected into HeLa cells, and the cells were exposed to (60)Co-irradiation at 24 h after transfection. The changes of Chk1/2 protein expression were assayed by Western blot and confocal laser scanning microscopy (Confocal), and the cell cycles, apoptosis rates and cell cycle specific apoptosis were detected by annexin V-PI labeling and flow cytometry.

RESULTSApoptotic response was significantly increased in the Hela cells after G(2)/M arrest and was inversed to activation of G(2)/M checkpoint. Either Chk1 or Chk2-specific AsODN consistently enhanced DNA damage-induced apoptosis by 90% approximately 120%, compared to corresponding sODN control (P < 0.05). Unexpectedly, combined use of Chk1- and Chk2-specific AsODN did not produce synergistic effect as compared to treatment with Chk1- or Chk2-specific AsODN alone (P > 0.05). While irradiated HeLa cells underwent apoptosis preferentially in G(1)-phase, apoptosis occurred in either of G(1)-, S- or G(2)/M -phase in the presence of Chk1 and/or Chk2 AsODN.

CONCLUSIONThe radioresistance is mainly induced by activating the cell cycle checkpoint signal transduction pathway after irradiation, and abrogating of the key effector Chk1 and Chk2 may increase the apoptotic sensitivity to irradiation due to changes of the pattern of cell cycle specific apoptosis.

Apoptosis ; radiation effects ; Cell Cycle ; radiation effects ; Checkpoint Kinase 1 ; Checkpoint Kinase 2 ; Cobalt Radioisotopes ; Down-Regulation ; Gene Expression Regulation, Neoplastic ; HeLa Cells ; Humans ; Oligodeoxyribonucleotides, Antisense ; genetics ; Protein Kinases ; genetics ; metabolism ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Transfection

Radiation is the most useful treatment modality for cancer patients. It initiates a series of signal cascades such as DNA damage response (DDR) signaling for repairing damaged DNA, arresting the cell cycle, and inducing cell death. Until now, few genes have been found to be regulated by radiation, which explains the molecular mechanisms of cellular responses to radiation. Although the transcriptional changes caused by radiation have been widely investigated, little is known about the direct evidence for the transcriptional control of DDR-related genes. Here, we examined the radiosensitivity of two non-small cell lung cancer cell lines (H460 and H1299), which have different p53 status. We monitored the time-dependent changes of 24 DDR-related gene expressions via microarray analysis. Based on the basal expression levels and temporal patterns, we further classified 24 DDR-related genes into four subgroups. Then, we also addressed the protein levels of several DDR-related genes such as TopBP1, Chk1 and Chk2, confirming the results of microarray analysis. Together, these results indicate that the expression patterns of DDR-related genes are associated with radiosensitivity and with the p53 statuses of H460 and H1299, which adds to the understanding of the complex biological responses to radiation.
Adaptor Proteins, Signal Transducing/genetics ; Cell Cycle Proteins/genetics ; Cell Line, Tumor ; Cell Survival/radiation effects ; DNA Damage/*radiation effects ; DNA Repair Enzymes/genetics ; DNA-Binding Proteins/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/*radiation effects ; Humans ; Lung Neoplasms ; Radiation Tolerance/genetics ; Signal Transduction

The activation of nuclear factor-kappa B1 (NFkappaB1) in cancer cells may confer resistance to ionizing radiation (IR). To enhance the therapeutic efficiency of IR in lung cancer, we screened for microRNAs (miRNAs) that suppress NFkappaB1 and observed their effects on radiosensitivity in a human lung cancer cell line. From time series data of miRNA expression in gamma-irradiated H1299 human lung cancer cells, we found that the expression of miR-9 was inversely correlated with that of NFkappaB1. Overexpression of miR-9 down-regulated the level of NFkappaB1 in H1299 cells, and the surviving fraction of gamma-irradiated cells was decreased. Interestingly, let-7g also suppressed the expression of NFkappaB1, although there was no canonical target site for let-7g in the NFkappaB1 3' untranslated region. From these results, we conclude that the expression of miR-9 and let-7g could enhance the efficiency of radiotherapy for lung cancer treatment through the inhibition of NFkappaB1.
Base Sequence ; Cell Line, Tumor ; Cell Survival/genetics/radiation effects ; Gene Expression Profiling ; *Gene Expression Regulation, Neoplastic/radiation effects ; Humans ; Lung Neoplasms/genetics/metabolism ; MicroRNAs/genetics/*metabolism ; NF-kappa B p50 Subunit/genetics/*metabolism ; Radiation Tolerance/*genetics ; Radiation, Ionizing ; Sequence Alignment